Central Nervous System Depressants: A very loosely defined group of drugs that tend to reduce the activity of the central nervous system. The major groups included here are ethyl alcohol, anesthetics, hypnotics and sedatives, narcotics, and tranquilizing agents (antipsychotics and antianxiety agents).Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges.Central Nervous System Diseases: Diseases of any component of the brain (including the cerebral hemispheres, diencephalon, brain stem, and cerebellum) or the spinal cord.Central Nervous System Neoplasms: Benign and malignant neoplastic processes that arise from or secondarily involve the brain, spinal cord, or meninges.Nervous System: The entire nerve apparatus, composed of a central part, the brain and spinal cord, and a peripheral part, the cranial and spinal nerves, autonomic ganglia, and plexuses. (Stedman, 26th ed)Brain: The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.Myocardial Depressant Factor: A low molecular weight peptide of about 800-1000 having a negative inotropic effect. It is released into the circulation during experimental hemorrhagic pancreatitis, severe ischemia, and postoligemic shock.Central Nervous System Infections: Pathogenic infections of the brain, spinal cord, and meninges. DNA VIRUS INFECTIONS; RNA VIRUS INFECTIONS; BACTERIAL INFECTIONS; MYCOPLASMA INFECTIONS; SPIROCHAETALES INFECTIONS; fungal infections; PROTOZOAN INFECTIONS; HELMINTHIASIS; and PRION DISEASES may involve the central nervous system as a primary or secondary process.Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors.Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.Depression, Chemical: The decrease in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.Central Nervous System Viral Diseases: Viral infections of the brain, spinal cord, meninges, or perimeningeal spaces.Spinal Cord: A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.Vasculitis, Central Nervous System: Inflammation of blood vessels within the central nervous system. Primary vasculitis is usually caused by autoimmune or idiopathic factors, while secondary vasculitis is caused by existing disease process. Clinical manifestations are highly variable but include HEADACHE; SEIZURES; behavioral alterations; INTRACRANIAL HEMORRHAGES; TRANSIENT ISCHEMIC ATTACK; and BRAIN INFARCTION. (From Adams et al., Principles of Neurology, 6th ed, pp856-61)Central Nervous System Agents: A class of drugs producing both physiological and psychological effects through a variety of mechanisms. They can be divided into "specific" agents, e.g., affecting an identifiable molecular mechanism unique to target cells bearing receptors for that agent, and "nonspecific" agents, those producing effects on different target cells and acting by diverse molecular mechanisms. Those with nonspecific mechanisms are generally further classed according to whether they produce behavioral depression or stimulation. Those with specific mechanisms are classed by locus of action or specific therapeutic use. (From Gilman AG, et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p252)Pentobarbital: A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236)Central Nervous System Fungal Infections: MYCOSES of the brain, spinal cord, and meninges which may result in ENCEPHALITIS; MENINGITIS, FUNGAL; MYELITIS; BRAIN ABSCESS; and EPIDURAL ABSCESS. Certain types of fungi may produce disease in immunologically normal hosts, while others are classified as opportunistic pathogens, causing illness primarily in immunocompromised individuals (e.g., ACQUIRED IMMUNODEFICIENCY SYNDROME).Meprobamate: A carbamate with hypnotic, sedative, and some muscle relaxant properties, although in therapeutic doses reduction of anxiety rather than a direct effect may be responsible for muscle relaxation. Meprobamate has been reported to have anticonvulsant actions against petit mal seizures, but not against grand mal seizures (which may be exacerbated). It is used in the treatment of ANXIETY DISORDERS, and also for the short-term management of INSOMNIA but has largely been superseded by the BENZODIAZEPINES. (From Martindale, The Extra Pharmacopoeia, 30th ed, p603)Enteric Nervous System: Two ganglionated neural plexuses in the gut wall which form one of the three major divisions of the autonomic nervous system. The enteric nervous system innervates the gastrointestinal tract, the pancreas, and the gallbladder. It contains sensory neurons, interneurons, and motor neurons. Thus the circuitry can autonomously sense the tension and the chemical environment in the gut and regulate blood vessel tone, motility, secretions, and fluid transport. The system is itself governed by the central nervous system and receives both parasympathetic and sympathetic innervation. (From Kandel, Schwartz, and Jessel, Principles of Neural Science, 3d ed, p766)Sympathetic Nervous System: The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system.Nervous System Physiological Phenomena: Characteristic properties and processes of the NERVOUS SYSTEM as a whole or with reference to the peripheral or the CENTRAL NERVOUS SYSTEM.Autonomic Nervous System: The ENTERIC NERVOUS SYSTEM; PARASYMPATHETIC NERVOUS SYSTEM; and SYMPATHETIC NERVOUS SYSTEM taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the CENTRAL NERVOUS SYSTEM, especially the HYPOTHALAMUS and the SOLITARY NUCLEUS, which receive information relayed from VISCERAL AFFERENTS.Nervous System Diseases: Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.Neuroglia: The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.Central Nervous System Bacterial Infections: Bacterial infections of the brain, spinal cord, and meninges, including infections involving the perimeningeal spaces.Barbiturates: A class of chemicals derived from barbituric acid or thiobarbituric acid. Many of these are GABA MODULATORS used as HYPNOTICS AND SEDATIVES, as ANESTHETICS, or as ANTICONVULSANTS.Myelin Sheath: The lipid-rich sheath surrounding AXONS in both the CENTRAL NERVOUS SYSTEMS and PERIPHERAL NERVOUS SYSTEM. The myelin sheath is an electrical insulator and allows faster and more energetically efficient conduction of impulses. The sheath is formed by the cell membranes of glial cells (SCHWANN CELLS in the peripheral and OLIGODENDROGLIA in the central nervous system). Deterioration of the sheath in DEMYELINATING DISEASES is a serious clinical problem.Blood-Brain Barrier: Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.Astrocytes: A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.Tuberculosis, Central Nervous System: Tuberculosis of the brain, spinal cord, or meninges (TUBERCULOSIS, MENINGEAL), most often caused by MYCOBACTERIUM TUBERCULOSIS and rarely by MYCOBACTERIUM BOVIS. The infection may be limited to the nervous system or coexist in other organs (e.g., TUBERCULOSIS, PULMONARY). The organism tends to seed the meninges causing a diffuse meningitis and leads to the formation of TUBERCULOMA, which may occur within the brain, spinal cord, or perimeningeal spaces. Tuberculous involvement of the vertebral column (TUBERCULOSIS, SPINAL) may result in nerve root or spinal cord compression. (From Adams et al., Principles of Neurology, 6th ed, pp717-20)Nervous System Neoplasms: Benign and malignant neoplastic processes arising from or involving components of the central, peripheral, and autonomic nervous systems, cranial nerves, and meninges. Included in this category are primary and metastatic nervous system neoplasms.Nerve Tissue ProteinsHypnotics and Sedatives: Drugs used to induce drowsiness or sleep or to reduce psychological excitement or anxiety.Demyelinating Diseases: Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system.Rats, Sprague-Dawley: A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Encephalomyelitis, Autoimmune, Experimental: An experimental animal model for central nervous system demyelinating disease. Inoculation with a white matter emulsion combined with FREUND'S ADJUVANT, myelin basic protein, or purified central myelin triggers a T cell-mediated immune response directed towards central myelin. The pathologic features are similar to MULTIPLE SCLEROSIS, including perivascular and periventricular foci of inflammation and demyelination. Subpial demyelination underlying meningeal infiltrations also occurs, which is also a feature of ENCEPHALOMYELITIS, ACUTE DISSEMINATED. Passive immunization with T-cells from an afflicted animal to a normal animal also induces this condition. (From Immunol Res 1998;17(1-2):217-27; Raine CS, Textbook of Neuropathology, 2nd ed, p604-5)Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.Oligodendroglia: A class of large neuroglial (macroglial) cells in the central nervous system. Oligodendroglia may be called interfascicular, perivascular, or perineuronal (not the same as SATELLITE CELLS, PERINEURONAL of GANGLIA) according to their location. They form the insulating MYELIN SHEATH of axons in the central nervous system.Brain Diseases: Pathologic conditions affecting the BRAIN, which is composed of the intracranial components of the CENTRAL NERVOUS SYSTEM. This includes (but is not limited to) the CEREBRAL CORTEX; intracranial white matter; BASAL GANGLIA; THALAMUS; HYPOTHALAMUS; BRAIN STEM; and CEREBELLUM.Scorpion Venoms: Venoms from animals of the order Scorpionida of the class Arachnida. They contain neuro- and hemotoxins, enzymes, and various other factors that may release acetylcholine and catecholamines from nerve endings. Of the several protein toxins that have been characterized, most are immunogenic.Enflurane: An extremely stable inhalation anesthetic that allows rapid adjustments of anesthesia depth with little change in pulse or respiratory rate.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Anesthetics: Agents that are capable of inducing a total or partial loss of sensation, especially tactile sensation and pain. They may act to induce general ANESTHESIA, in which an unconscious state is achieved, or may act locally to induce numbness or lack of sensation at a targeted site.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Cerebrospinal Fluid: A watery fluid that is continuously produced in the CHOROID PLEXUS and circulates around the surface of the BRAIN; SPINAL CORD; and in the CEREBRAL VENTRICLES.Gene Expression Regulation, Developmental: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes.Multiple Sclerosis: An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)Cats: The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)Metergoline: A dopamine agonist and serotonin antagonist. It has been used similarly to BROMOCRIPTINE as a dopamine agonist and also for MIGRAINE DISORDERS therapy.Brain Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.Mice, Inbred C57BLEncephalomyelitis: A general term indicating inflammation of the BRAIN and SPINAL CORD, often used to indicate an infectious process, but also applicable to a variety of autoimmune and toxic-metabolic conditions. There is significant overlap regarding the usage of this term and ENCEPHALITIS in the literature.Cerebral Cortex: The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Microglia: The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.Encephalitis: Inflammation of the BRAIN due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see ENCEPHALITIS, VIRAL) are a relatively frequent cause of this condition.Encephalitis, Viral: Inflammation of brain parenchymal tissue as a result of viral infection. Encephalitis may occur as primary or secondary manifestation of TOGAVIRIDAE INFECTIONS; HERPESVIRIDAE INFECTIONS; ADENOVIRIDAE INFECTIONS; FLAVIVIRIDAE INFECTIONS; BUNYAVIRIDAE INFECTIONS; PICORNAVIRIDAE INFECTIONS; PARAMYXOVIRIDAE INFECTIONS; ORTHOMYXOVIRIDAE INFECTIONS; RETROVIRIDAE INFECTIONS; and ARENAVIRIDAE INFECTIONS.Brain Stem: The part of the brain that connects the CEREBRAL HEMISPHERES with the SPINAL CORD. It consists of the MESENCEPHALON; PONS; and MEDULLA OBLONGATA.Synaptic Transmission: The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.Meningoencephalitis: An inflammatory process involving the brain (ENCEPHALITIS) and meninges (MENINGITIS), most often produced by pathogenic organisms which invade the central nervous system, and occasionally by toxins, autoimmune disorders, and other conditions.Desipramine: A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholinergic activity, through its affinity to muscarinic receptors.Iontophoresis: Therapeutic introduction of ions of soluble salts into tissues by means of electric current. In medical literature it is commonly used to indicate the process of increasing the penetration of drugs into surface tissues by the application of electric current. It has nothing to do with ION EXCHANGE; AIR IONIZATION nor PHONOPHORESIS, none of which requires current.Halothane: A nonflammable, halogenated, hydrocarbon anesthetic that provides relatively rapid induction with little or no excitement. Analgesia may not be adequate. NITROUS OXIDE is often given concomitantly. Because halothane may not produce sufficient muscle relaxation, supplemental neuromuscular blocking agents may be required. (From AMA Drug Evaluations Annual, 1994, p178)Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or "seizure disorder."Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking DOPAMINE RECEPTORS. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup.Brain Chemistry: Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states.Aminobutyrates: Derivatives of BUTYRIC ACID that contain one or more amino groups attached to the aliphatic structure. Included under this heading are a broad variety of acid forms, salts, esters, and amides that include the aminobutryrate structure.Trauma, Nervous System: Traumatic injuries to the brain, cranial nerves, spinal cord, autonomic nervous system, or neuromuscular system, including iatrogenic injuries induced by surgical procedures.Electric Stimulation: Use of electric potential or currents to elicit biological responses.Muscle Relaxants, Central: A heterogeneous group of drugs used to produce muscle relaxation, excepting the neuromuscular blocking agents. They have their primary clinical and therapeutic uses in the treatment of muscle spasm and immobility associated with strains, sprains, and injuries of the back and, to a lesser degree, injuries to the neck. They have been used also for the treatment of a variety of clinical conditions that have in common only the presence of skeletal muscle hyperactivity, for example, the muscle spasms that can occur in MULTIPLE SCLEROSIS. (From Smith and Reynard, Textbook of Pharmacology, 1991, p358)Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Myelin Proteins: MYELIN-specific proteins that play a structural or regulatory role in the genesis and maintenance of the lamellar MYELIN SHEATH structure.Isoflurane: A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.Respiration: The act of breathing with the LUNGS, consisting of INHALATION, or the taking into the lungs of the ambient air, and of EXHALATION, or the expelling of the modified air which contains more CARBON DIOXIDE than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= OXYGEN CONSUMPTION) or cell respiration (= CELL RESPIRATION).Hippocampus: A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Morphine: The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle.Peripheral Nerves: The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium.Heart Rate: The number of times the HEART VENTRICLES contract per unit of time, usually per minute.Motor Activity: The physical activity of a human or an animal as a behavioral phenomenon.Bemegride: A CNS stimulant that is used to induce convulsions in experimental animals. It has also been used as a respiratory stimulant and in the treatment of barbiturate overdose.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Animals, Newborn: Refers to animals in the period of time just after birth.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Injections, Intraventricular: Injections into the cerebral ventricles.Synapses: Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate via direct electrical coupling with ELECTRICAL SYNAPSES. Several other non-synaptic chemical or electric signal transmitting processes occur via extracellular mediated interactions.Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.Behavior, Animal: The observable response an animal makes to any situation.Diazepam: A benzodiazepine with anticonvulsant, anxiolytic, sedative, muscle relaxant, and amnesic properties and a long duration of action. Its actions are mediated by enhancement of GAMMA-AMINOBUTYRIC ACID activity.Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.Cerebellum: The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Meninges: The three membranes that cover the BRAIN and the SPINAL CORD. They are the dura mater, the arachnoid, and the pia mater.Nerve Regeneration: Renewal or physiological repair of damaged nerve tissue.Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.

Ciprofloxacin decreases the rate of ethanol elimination in humans. (1/1532)

BACKGROUND: Extrahepatic ethanol metabolism is postulated to take place via microbial oxidation in the colon, mediated by aerobic and facultative anaerobic bacteria. AIMS: To evaluate the role of microbial ethanol oxidation in the total elimination rate of ethanol in humans by reducing gut flora with ciprofloxacin. METHODS: Ethanol was administered intravenously at the beginning and end of a one week period to eight male volunteers. Between ethanol doses volunteers received 750 mg ciprofloxacin twice daily. RESULTS: A highly significant (p=0.001) reduction in the ethanol elimination rate (EER) was detected after ciprofloxacin medication. Mean (SEM) EER was 107.0 (5.3) and 96.9 (4.8) mg/kg/h before and after ciprofloxacin, respectively. Faecal Enterobacteriaceae and Enterococcus sp. were totally absent after medication, and faecal acetaldehyde production capacity was significantly (p<0.05) decreased from 0.91 (0.15) to 0.39 (0.08) nmol/min/mg protein. Mean faecal alcohol dehydrogenase (ADH) activity was significantly (p<0. 05) decreased after medication, but ciprofloxacin did not inhibit human hepatic ADH activity in vitro. CONCLUSIONS: Ciprofloxacin treatment decreased the ethanol elimination rate by 9.4%, with a concomitant decrease in intestinal aerobic and facultative anaerobic bacteria, faecal ADH activity, and acetaldehyde production. As ciprofloxacin has no effect on liver blood flow, hepatic ADH activity, or cytochrome CYP2E1 activity, these effects are probably caused by the reduction in intestinal flora.  (+info)

Acute effects of ethanol on kainate receptors with different subunit compositions. (2/1532)

Previous studies showed that recombinant homomeric GluR6 receptors are acutely inhibited by ethanol. This study examined the acute actions of ethanol on recombinant homomeric and heteromeric kainate (KA) receptors with different subunit configurations. Application of 25 to 100 mM ethanol produced inhibition of a similar magnitude of both GluR5-Q and GluR6-R KA receptor-dependent currents in Xenopus oocytes. Ethanol decreased the KA Emax without affecting the EC50 and its effect was independent of the membrane holding potential for both of these receptors subtypes. Ethanol also inhibited homomeric and heteromeric receptors transiently expressed in human embryonic kidney (HEK) 293 cells. In these cells, the expression of heteromeric GluR6-R subunit-containing receptors was confirmed by testing their sensitivity to 1 mM alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid. Ethanol inhibited to a similar extent KA-gated currents mediated by receptors composed of either GluR6 or GluR6 + KA1 subunits, and to a slightly lesser extent receptors composed of GluR6 + KA2 subunits. Acute ethanol's effects were tested on GluR5 KA receptors that are expressed as homomers (GluR5-Q) or heteromers (GluR5-R + KA1 and GluR5-R + KA2). Homomeric and heteromeric GluR5 KA receptors were all inhibited to a similar extent by ethanol; however, there was slightly more inhibition of GluR5-R + KA2 receptors. Thus, recombinant KA receptors with different subunit compositions are all acutely inhibited to a similar extent by ethanol. In light of recent reports that KA receptors regulate neurotransmitter release and mediate synaptic currents, we postulate that these receptors may play a role in acute ethanol intoxication.  (+info)

NMDA receptor characterization and subunit expression in rat cultured mesencephalic neurones. (3/1532)

1. NMDA-induced changes in free intracellular Ca2+ concentration ([Ca2+]i) were determined in individual cultured rat mesencephalic neurones by the fura-2 method. mRNA expression encoding NMDA receptor subunits (NR1, NR2A-D) was examined by RT-PCR. 2. NMDA (1-100 microM, plus 10 microM glycine) induced a concentration-dependent increase in [Ca2+]i (EC50 = 5.7 microM). The effect of NMDA was virtually insensitive to tetrodotoxin (0.3 microM) and nitrendipine (1 microM), but dependent on extracellular Ca2+. 5,7-Dichlorokynurenic acid (10 microM), a specific antagonist at the glycine binding site on the NMDA receptor, abolished the NMDA response. 3. Memantine, an open-channel blocker, and ifenprodil, a preferential non-competitive NR1/NR2B receptor antagonist diminished the NMDA effect with an IC50 value of 0.17 and 1 microM, respectively. Ethanol at 50 and 100 mM caused about 25 and 45%-inhibition, respectively. 4. Agarose gel analysis of the PCR products followed by ethidium bromide fluorescence or CSPD chemiluminescence detection revealed an almost exclusive expression of the NR1 splice variants lacking exon (E) 5 and E22. The 3' splice form without both E21 and E22 exceeded that containing E21 by approximately 4 fold. The relative amounts of NR2A, NR2B, NR2C corresponded to approximately 1:2:1. NR2D mRNA was also detectable. 5. In conclusion, mesencephalic neurones bear ethanol-sensitive NMDA receptors which might be involved in the development of ethanol dependence and withdrawal. The high affinity of NMDA to this receptor, its sensitivity to ifenprodil and memantine may suggest that the mesencephalic NMDA receptor comprises the NR1 splice variant lacking E5, NR2B, and NR2C, respectively.  (+info)

Effects of alcohol and cholesterol feeding on lipoprotein metabolism and cholesterol absorption in rabbits. (4/1532)

Alcohol fed to rabbits in a liquid formula at 30% of calories increased plasma cholesterol by 36% in the absence of dietary cholesterol and by 40% in the presence of a 0.5% cholesterol diet. The increase was caused almost entirely by VLDL, IDL, and LDL. Cholesterol feeding decreased the fractional catabolic rate for VLDL and LDL apoprotein by 80% and 57%, respectively, and increased the production rate of VLDL and LDL apoprotein by 75% and 15%, respectively. Alcohol feeding had no effect on VLDL apoprotein production but increased LDL production rate by 55%. The efficiency of intestinal cholesterol absorption was increased by alcohol. In the presence of dietary cholesterol, percent cholesterol absorption rose from 34.4+/-2.6% to 44.9+/-2.5% and in the absence of dietary cholesterol, from 84.3+/-1.4% to 88.9+/-1.0%. Increased cholesterol absorption and increased LDL production rate may be important mechanisms for exacerbation by alcohol of hypercholesterolemia in the cholesterol-fed rabbit model.  (+info)

Mode of action of ICS 205,930, a novel type of potentiator of responses to glycine in rat spinal neurones. (5/1532)

The effect of a novel potentiator of glycine responses, ICS 205,930, was studied by whole-cell recordings from spinal neurones, and compared with that of other known potentiators, in an attempt to differentiate their sites of action. The ability of ICS 205,930 (0.2 microM) to potentiate glycine responses persisted in the presence of concentrations of Zn2+ (5-10 microM) that were saturating for the potentiating effect of this ion. Preincubation with 10 microM Zn2+ before application of glycine plus Zn2+ had an inhibitory effect, which did not result from Zn2+ entry into the neurone, since it persisted with either 10 mM internal EGTA or 10 microM internal Zn2+. To test whether the potentiating effects of ICS 205,930 and Zn2+ interact, both compounds were applied without preincubation. The potentiating effect of ICS 205,930 was similar for responses to glycine and for responses to glycine plus Zn2+, provided the concentrations of agonist were adjusted so as to induce control responses of identical amplitudes. ICS 205,930 remained able to potentiate glycine responses in the presence of ethanol (200 mM). ICS 205,930 also retained its potentiating effect in the presence of the anaesthetic propofol (30 90 microM), which strongly potentiated glycine responses but, in contrast with ICS 205,930, also markedly increased the resting conductance. The anticonvulsant chlormethiazole (50-100 microM) neither potentiated glycine responses nor prevented the effect of ICS 205,930, even though it increased the resting conductance and potentiated GABA(A) responses. The mechanism of action of ICS 205,930 appears to be different from those by which Zn2+, propofol or ethanol potentiate glycine responses.  (+info)

Sweat ethanol concentrations are highly correlated with co-existing blood values in humans. (6/1532)

This study compared the concentration of ethanol, both absolute and relative to water content, in sweat and blood. Ten male volunteers consumed approximately 13 mmol (kg body weight)-1 of ethanol. Blood and sweat samples were collected approximately 1, 2 and 3 h following ingestion. Sweat was collected following pilocarpine iontophoresis using an anaerobic technique that prevented ethanol evaporation. In addition, the water content of sweat and blood samples was determined. The correlation between sweat and blood ethanol, expressed in mmol l-1, was r = 0.98. The slope of the relationship was 0.81. When corrected for the water content in each sample, and expressed as mmoles per litre of water, the correlation remained very high (r = 0.97) while the slope increased to 1.01. These results suggest that rapid and complete equilibrium of ethanol occurs across the sweat gland epithelium.  (+info)

Diffusion of dialkylnitrosamines into the rat esophagus as a factor in esophageal carcinogenesis. (7/1532)

To indicate how readily nitrosamines (NAms) diffuse into the esophagus, we measured diffusion rate (flux) through rat esophagus of dialkyl-NAms using side-by-side diffusion apparatuses. Mucosal and serosal flux at 37 degrees C of two NAms, each at 50 microM, was followed for 90 min by gas chromatography-thermal energy analysis of NAms in the receiver chamber. Mucosal flux of one or two NAms at a time gave identical results. Mucosal flux was highest for the strong esophageal carcinogens methyl-n-amyl-NAm (MNAN) and methylbenzyl-NAm. Mucosal esophageal flux of 11 NAms was 18-280 times faster and flux of two NAms through skin was 13-28 times faster than that predicted for skin from the molecular weights and octanol:water partition coefficients, which were also measured. Mucosal: serosal flux ratio was correlated (P < 0.05) with esophageal carcinogenicity and molecular weight. For seven NAms tested for carcinogenicity by Druckrey et al. [(1967) Z. Krebsforsch., 69, 103-201], mucosal flux was correlated with esophageal carcinogenicity with borderline significance (P = 0.07). The MNAN:dipropyl-NAm ratio for mucosal esophageal flux was unaffected when rats were treated with phenethylisothiocyanate and was similar to that for forestomach, indicating no involvement by cytochromes P450. Mucosal esophageal flux of MNAN and dimethyl-NAm was reduced by >90% on enzymic removal of the stratum corneum, was unaffected by 0.1 mM verapamil and was inhibited 67-94% by 1.0 mM KCN and 82-93% by 0.23% ethanol. NAm flux through rat skin and jejunum was 5-17% of that through esophagus. Flux through skin increased 5-13 times after enzymic or mechanical removal of the epidermis; the histology probably explained this difference from esophagus. Hence, NAms could be quite rapidly absorbed by human esophagus when NAm-containing foods or beverages are swallowed, the esophageal carcinogenicity of NAms may be partly determined by their esophageal flux and NAm flux probably occurs by passive diffusion.  (+info)

Dental anesthetic management of a patient with ventricular arrhythmias. (8/1532)

During routine deep sedation for endodontic therapy, a dentist-anesthesiologist observed premature ventricular contractions (PVCs) on a 62-yr-old woman's electrocardiogram (EKG) tracing. The dentist was able to complete the root canal procedure under intravenous (i.v.) sedation without any problems. The dentist-anesthesiologist referred the patient for medical evaluation. She was found to be free from ischemic cardiac disease with normal ventricular function. The patient was cleared to continue her dental treatment with deep sedation. She subsequently continued to undergo dental treatment with deep intravenous sedation without incident, although her EKG exhibited frequent PVCs, up to 20 per minute, including couplets and episodes of trigeminy. This article will review indications for medical intervention, antiarrhythmic medications, and anesthetic interventions for perioperative PVCs.  (+info)

*Chlormezanone

Sterling Drug Inc., US 3082209 (1958). Surrey, A. R.; Webb, W. G.; Gesler, R. M. (1958). "Central Nervous System Depressants. ... Seeling A, Oelschläger H, Rothley D (2000). "Important pharmaceutical-chemical characteristics of the central muscle relaxant ... Cleavage and biotransformation of the central muscle relaxant chlormezanone]". Pharmazie. 53 (9): 620-4. PMID 9770210. Gautier ...

*Carbamic acid

2004). "Central Nervous System Depressant". Wilson and Gisvold's textbook of organic medicinal and pharmaceutical chemistry. ...

*Corvalol

Phenobarbital is a central nervous system depressant. According to the Farmak product label of Colvalol oral solution, the ... Symptoms of overdose include central nervous system depression, confusion, dizziness, ataxia, and somnolence. In serious cases ... Corvalol may increase CNS depressant effect of other sedatives and hypnotics. Corvalol belongs to the sedative-hypnotic ... nervous asthma, hysterical states, excitability, hypochondria, headaches, migraine, menstrual cramps and symptoms associated ...

*Diazepam

The impairment is worsened by consumption of alcohol, because both act as central nervous system depressants. During the course ... Concomitant use of other central nervous system depressants increases this risk. The smallest possible effective dose should be ... As a result, the arousal of the cortical and limbic systems in the central nervous system is reduced. The GABAA receptor is a ... Diazepam binding in mammalian central nervous system: a pharmacological characterization". The Journal of Neuroscience. 1 (2): ...

*Anticonvulsant

Barbiturates are drugs that act as central nervous system (CNS) depressants, and by virtue of this they produce a wide spectrum ... Benzodiazepines act as a central nervous system depressant. The relative strength of each of these properties in any given ... Next to the voltage-gated sodium channels and components of the GABA system, their targets include GABAA receptors, the GAT-1 ... and voltage-dependent limitation of high frequency repetitive firing of action potentials of mouse central neurons in cell ...

*Ethyl formate

... and the respiratory system of humans and other animals; it is also a central nervous system depressant. In industry, it is used ... Department of Agriculture quarantine system) OSHA considers a time-weighted average of 100 parts per million (300 milligrams ...

*Tizanidine

... has the potential to interact with other central nervous system depressants. Alcohol should be avoided, particularly ... or certain other injuries to the spine or central nervous system. It is also prescribed off-label for migraine headaches, as a ... The CNS-depressant effects of tizanidine and alcohol are additive. It has a volume of distribution of 2.4 L/kg following ...

*Date rape drug

Gamma-hydroxybutyrate (GHB) is a central nervous system depressant. It has no odor, tastes salty, but is detectable when mixed ...

*Clonazolam

... benzodiazepines which have central nervous system depressant activity". Journal of Medicinal Chemistry. 14 (11): 1078-1081. doi ...

*Benzodiazepine

When combined with other central nervous system (CNS) depressants such as alcoholic drinks and opioids, the potential for ... Taking benzodiazepines with alcohol, opioids and other central nervous system depressants potentiates their action. This often ... and to a lesser extent the central nervous system. These peripheral receptors are not structurally related or coupled to GABAA ... Peripheral benzodiazepine receptors are present in peripheral nervous system tissues, glial cells, ...

*Meclizine

It possesses anticholinergic, central nervous system depressant, and local anesthetic effects. Its antiemetic and antivertigo ... effects are not fully understood, but its central anticholinergic properties are partially responsible. The drug depresses ...

*Diazepam

The impairment is worsened by consumption of alcohol, because both act as central nervous system depressants.[22] ... Concomitant use of other central nervous system depressants increases this risk. The smallest possible effective dose should be ... As a result, the arousal of the cortical and limbic systems in the central nervous system is reduced.[3] ... Diazepam binding in mammalian central nervous system: a pharmacological characterization". The Journal of Neuroscience. 1 (2): ...

*Drug Recognition Expert

Central Nervous System depressants (Benzodiazepines), CNS stimulants (Methamphetamine), Dissociative anesthetics (PCP), ...

*Propene

... acts as a central nervous system depressant via allosteric agonism of the GABAA receptor. Excessive exposure may result ...

*Cyclobenzaprine

The potential harm is increased when central nervous system depressants and antidepressants are also used; deliberate overdose ... These substances may interact with cyclobenzaprine: Central nervous system depressants (e.g. alcohol, opioids, benzodiazepines ...

*Effects of alcohol on memory

Alcohol acts as a general central nervous system depressant, but it also affects specific areas of the brain to a greater ... It is a volatile, flammable, colorless liquid that acts as a central nervous system depressant. Ethanol can impair different ... Since alcohol affects the central nervous system, it hinders semantic storage functioning by restricting the consolidation of ... has an inhibitory effect on neurotransmission in the central nervous system. GABAA receptor subtypes vary in their sensitivity ...

*Triazolam

... (original brand name Halcion) is a central nervous system (CNS) depressant in the benzodiazepine class. It possesses ...

*Pregabalin

In clinical studies, pregabalin showed a side effect profile similar to other central nervous system depressants. Adverse drug ... and central neuropathic pain. A minority obtain substantial benefit, and a larger number obtain moderate benefit. Other first ...

*Baclofen

It is used as a central nervous system depressant and skeletal muscle relaxant. It is also used in topical creams to help with ... "Baclofen". The American Society of Health-System Pharmacists. Retrieved 2011-12-06. Leggio, L.; Garbutt, J. C.; Addolorato, G ... are designed to deliver the medication directly to the spinal fluid rather than going through the digestive and blood system ...

*Fioricet

Butalbital has generalized depressant effect on central nervous system and, in very high doses, has peripheral effects. ...

*Lorazepam

Sleep apnea - Sleep apnea may be worsened by lorazepam's central nervous system depressant effects. It may further reduce the ... may depress central nervous system respiratory drive and are contraindicated in severe respiratory failure. An example would be ... American Society of Health-System Pharmacists. June 29, 2016. Archived from the original on 5 June 2016. Retrieved 15 July 2016 ... Lorazepam's anticonvulsant and CNS depressant properties are useful for the treatment and prevention of alcohol withdrawal ...

*Nitrazolam

... benzodiazepines which have central nervous system depressant activity". Journal of Medicinal Chemistry. 14 (11): 1078-1081. doi ...

*Flubromazolam

... benzodiazepines which have central nervous system depressant activity". Journal of Medicinal Chemistry. 14 (11): 1078-1081. doi ...

*Pergularia

... anti-infertility and central nervous system depressant activity. Species Pergularia adenophylla Schltr. & K. Schum. - Cameroon ...

*Orange Valley Regional Groundwater Superfund site

It is also a known central nervous system depressant and can dissolves fats from the skin, causing skin irritation. There is ... DCE targets the skin, liver, kidneys, lungs, and central nervous system, in which exposure can result in irritation of the skin ... and central nervous system depression. In the early 1980s, when the contamination was first discovered, the Orange Water ... humans by all routes of exposure and poses a potential human health hazard for noncancer toxicity to the central nervous system ...

*Ethyl acetate

Animal experiments have shown that, at very high concentrations, the ester has central nervous system depressant and lethal ... symptoms of central nervous system depression, secondary anemia and liver damage. In humans, concentrations of 400 ppm cause ...

*GABAA receptor positive allosteric modulator

Neurosteroids are synthesized in the central nervous system (CNS) and the peripheral nervous system (PNS) from cholesterol and ... S(-) form of barbiturate have shown more depressant activity while the R(+) isomers have an excitatory effect.[28] ... Baulieu EE (1997). "Neurosteroids: of the nervous system, by the nervous system, for the nervous system". Recent Progress in ... GABA is a major inhibitory neurotransmitter in the central nervous system. Upon binding, it triggers the GABAA receptor to open ...

*Xylazine

Results from early human clinical studies confirmed that xylazine has several central nervous system depressant effects. ... which are physiological antagonists to central nervous system depressants. Combining yohimbine and 4-aminopyridine in an effort ... As an agonist, xylazine leads to a decrease in neurotransmission of norepinephrine and dopamine in the central nervous system. ... The sedative and analgesic effects of xylazine are related to central nervous system depression. Xylazine's muscle relaxant ...
The most commonly abused prescription drugs among teenagers are opioids, central nervous system depressants, and stimulants - like Roxies.
TY - JOUR. T1 - Stable histone methylation changes at proteoglycan network genes following ethanol exposure. AU - Gavin, David P.. AU - Hashimoto, Joel G.. AU - Lazar, Nathan H.. AU - Carbone, Lucia. AU - Crabbe, John Jr. AU - Guizzetti, Marina. PY - 2018/8/30. Y1 - 2018/8/30. N2 - Alcohol use disorder (AUD) is a chronic mental illness in which patients often achieve protracted periods of abstinence prior to relapse. Epigenetic mechanisms may provide an explanation for the persisting gene expression changes that can be observed even after long periods of abstinence and may contribute to relapse. In this study, we examined two histone modifications, histone 3 lysine 4 tri-methylation (H3K4me3) and histone 3 lysine 27 tri-methylation (H3K27me3), in the prefrontal cortex of Withdrawal Seizure Resistant (WSR) mice 21 days after 72 h of ethanol vapor exposure. These histone modifications were selected because they are associated with active promoters (H3K4me3) and repressed gene expression in a ...
The Ethanol Effect is the newest hour-long special from the team behind Detroit Public Televisions Alfred I. DuPont/Columbia University Award-winning series Beyond the Light Switch.. From Iowas farm fields to Washingtons corridors of power, and from the algae-choked surface of the Great Lakes to the poisoned depths of the Gulf of Mexico, The Ethanol Effect investigates the human, environmental and political costs of growing and refining corn for ethanol in America. Our guide through the tangled web of ethanols influence is David Biello. Follow Biello as he untangles the web of ethanols unexpected influence on our daily in The Ethanol Effect ...
The Ethanol Effect is the newest hour-long special from the team behind Detroit Public Televisions Alfred I. DuPont/Columbia University Award-winning series Beyond the Light Switch.. From Iowas farm fields to Washingtons corridors of power, and from the algae-choked surface of the Great Lakes to the poisoned depths of the Gulf of Mexico, The Ethanol Effect investigates the human, environmental and political costs of growing and refining corn for ethanol in America. Our guide through the tangled web of ethanols influence is David Biello. Follow Biello as he untangles the web of ethanols unexpected influence on our daily in The Ethanol Effect ...
The present article provides an up-to-date review summarizing almost 18 years of research in genetically selected Marchigian Sardinian alcohol-preferring (msP) rats. The results of this work demonstrate that msP rats have natural preference for ethanol characterized by a spontaneous binge-type of drinking that leads to pharmacologically significant blood ethanol levels. This rat line is highly vulnerable to relapse and presentation of stimuli predictive of alcohol availability or foot-shock stress can reinstate extinguished drug-seeking up to 8 months from the last alcohol experience. The msP rat is highly sensitive to stress, shows an anxious phenotype and has depressive-like symptoms that recover following ethanol drinking. Interestingly, these animals have an up-regulated corticotrophin releasing factor (CRF) receptor 1 system. Clinical studies have shown that alcoholic patients often drink ethanol in the attempt to self-medicate from negative affective states and to search for anxiety ...
TY - JOUR. T1 - Subcellular location of secretory proteins retained in the liver during the ethanol-induced inhibition of hepatic protein secretion in the rat. AU - Volentine, Gary D. AU - Tuma, Dean J. AU - Sorrell, Michael Floyd. PY - 1986/1/1. Y1 - 1986/1/1. N2 - Ethanol administration inhibits the secretion of proteins by the liver, resulting in their hepatocellular retention. Experiments were designed in this study to determine the subcellular location of the retained secretory proteins. Ethanol was administered acutely to nonfasted rats by gastric intubation, whereas control animals received an isocaloric dose of glucose. Two hours after intubation, when maximum blood ethanol levels (45 mM) were observed, [3H]leucine and [14C]fucose were injected simultaneously into the dorsal vein of the penis. The labeling of secretory proteins was determined in the liver and plasma at various time periods after label injection. Ethanol treatment decreased the secretion of both leucine- and ...
March 2013. Subjects. This model has been predominantly been studied using adult (65-75 days of age) male C57BL/6J mice obtained from Jackson Laboratories (Bar Harbor, ME). Although experimental parameters have been optimized using these mice, we have conducted studies with adult female C57BL/6J mice, as well as other inbred mouse strains including DBA/2J and C3H/Hecr, selectively bred HAP/LAP lines, and and BXD RI lines. Mice are acclimated to the facility for at least two weeks prior to experimental use. Mice are individually housed in standard polypropylene pans with wood-chip bedding and stainless steel wire lids. The mice are housed under a modified light/dark cycle (lights on at 0200 hr) to allow for behavioral testing to be conducted during the dark phase of the cycle. Rodent food (Wayne Lab-Blox) and water is available ad libitum at all times during the studies.. General Experimental Design and Strategy. The overall objective of this chronic intermittent ethanol (CIE) exposure model ...
Previous studies in mice and rats have shown that selective breeding for high and low ethanol preference results in divergence of circadian phenotype in the selected lines. These results indicate that some alleles influencing ethanol preference also contribute to circadian rhythm regulation. Selective breeding has also been used to produce lines of mice differing in a number of other ethanol-related traits, while studies of phenotypic and genetic correlation indicate that diverse ethanol-related traits are influenced by both shared and unshared genetics. ...
TY - JOUR. T1 - Body temperature differentially affects ethanol sensitivity in both inbred strains and selected lines of mice. AU - Finn, Deborah (Deb). AU - Bejanian, M.. AU - Jones, B. L.. AU - McGivern, R. F.. AU - Syapin, P. J.. AU - Crabbe, John Jr. AU - Alkana, R. L.. PY - 1990. Y1 - 1990. N2 - Offsetting ethanol-induced hypothermia in five inbred strains of mice changed ethanol sensitivity within strains and markedly reduced differences between strains in brain sensitivity to hypnotic ethanol doses. The present study extended this work to mice selectivity bred for sensitivity and resistance to ethanol-induced loss of righting reflex (LORR) and hypothermia. In all experiments LORR duration and ethanol concentrations at return of righting reflex were measured after i.p. hypnotic ethanol doses and exposure to 22 or 34°C. In experiment 1, C57BL/6J, A/HeJ, 129/J, LS/Ibg and SS/Ibg mice were given 4.2 g/kg ethanol. In experiment 2, the same mouse genotypes were tested with different ethanol ...
We use cookies to ensure that we give you the best experience on our website. If you click Continue well assume that you are happy to receive all cookies and you wont see this message again. Click Find out more for information on how to change your cookie settings ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Chronic alcohol exposure affects the central nervous system, influences behavior, and induces neuroadaptive changes in vertebrate species including our own. literature to be alcohol related. We conclude that the zebrafish is an excellent tool for the analysis of genes associated with alcohols actions in vertebrates, one which may facilitate the discovery and better understanding of […]. ...
How Does E85 Ethanol Affect You? - What is the effect of E85 ethanol flex fuel on the consumer? Learn the answer at HowStuffWorks, including why it is available in only some states.
The effects of ethanol on a fetus are extensive, devastating, and often permanent. Depending upon the population, ethanol affects as many as 2% of all live birt...
Study Flashcards On Nervous System Depressants and Muscle relaxants at Cram.com. Quickly memorize the terms, phrases and much more. Cram.com makes it easy to get the grade you want!
Alcohol affects a number of different biochemical pathways and a better understanding of the factors that contribute to alcohol abuse and addiction could lead to improved treatments. Since a lower initial response to the effects of alcohol has been found to correlate with increased risk of future alcoholism, identification of the genes and pathways involved in the acute response might throw light on the genetic factors contributing to addiction. The fruit fly, Drosophila melanogaster, reacts in much the same way as mammals to acute ethanol exposure and a team led by Ulrike Heberlein at the University of California is using the fly to explore the links between genetic make-up and response to alcohol. Their latest find is that flies with a mutant version of a gene that they have designated happyhour are less sensitive to the sedative effects of alcohol than flies with a normal copy of the gene. Further studies showed that the epidermal growth factor (EGF)-signalling pathway regulates ethanol ...
NEW YORK - A U.S. ethanol industry group is pushing lawmakers to craft legislation requiring fuel companies to inform customers what country their fuel came from in hopes of increasing awareness about money spent on oil imported from overseas.
A free platform for explaining your research in plain language, and managing how you communicate around it - so you can understand how best to increase its impact.
Intoxicated: 22-33 mmol/L (0.10-0.15 g/100 mL). Poisoned: 44-66 mmol/L (0.20-0.30 g/100 mL). Often fatal: , 88 mmol/L (, 0.40 g/100 mL).. Legal limits vary. For specific information contact local authorities.. Commonly, the legal driving limit is 0.05% that is, 11 mmol/L or 0.05 g/100 mL. In some regions it is 0.08% ,that is, 18 mmol/L or 0.08 g/100 mL.. ...
All of the costs associated of making ethanol are tied up in the cost of corn and grain and so if you are not careful with buying grain you can be in trouble fast.". While it seems like a lot of gloom and doom for the nations ethanol industry featuring grain and fuel price volatility. Those who study the industry say there is no way ethanol plants dont have a role in the future of alternative energy. "Ethanol has had wonderful times but have gone thru a dry spot the last 9 months but they have a rosy future.". Meantime the ethanol industry waits to see the impact of the corn harvest. Part of a cycle these plants live and die by.. "Not going away, in fact I think it will continue to grow. ...
Alcohol is a direct cause of seven forms of cancer. Tough words to swallow, but those are the conclusions of researchers from New Zealand, who say they found that no matter how much you drink, alcohol will increase your risk of cancer.
The number of air rage incidents has risen by nearly a third fuelled by drinking on flights, according to government figures.
Learn how drugs and alcohol cause physical changes to the brain that may lead to dependency or chronic addiction. Need help? Call 720.891.4657
Lumina Products - Ethanol | Non Ethanol Fuel Alternatives | Safety ProductsLumina Products | Ethanol | Non Ethanol Fuel Alternatives | Safety Products
... IN WATER WAS PREPARED HOW MANY GRAMS OF ETHANOL WOULD BE IN 100ML OF THE MIXTURE? (ASSUMING MIXED VOLUME IS THE SUM OF THE PARTIAL VOLUME) ...
Ethanol Facts - Learn about ethanol how it is made and the uses of Ethanol. Discover why ethanol is a very good sustainable fuel that used used in motor cars all over the world.
ethanol fireplace reviews splashy ethanol fireplace in living room contemporary with fireplace vase next to ethanol fireplace alongside condo ethanol fireplace insert reviews.. ...
Ethanol purity is important as even low levels of contaminants can have a significant effect on the ethanols behaviour. Ethanol is available as several different grades, with the most pure being 99.9 to 100 per cent pure. Specific applications require specific levels of purity.
2-(2,3,6-TRIFLUOROPHENOXY)ETHANOL chemical properties, What are the chemical properties of 2-(2,3,6-TRIFLUOROPHENOXY)ETHANOL 72912-49-3, What are the physical properties of 2-(2,3,6-TRIFLUOROPHENOXY)ETHANOL ect.
Anti Ethanol Anti Ethanol 07 za nejvýhodnější cenu. Vyberte si v nabídce Elnino.cz váš oblíbený parfém či kosmetiku. Doprava do 24 hodin.
Pacific Ethanol Inc. (PEIX) company profile: market capitalization, financial ratios, valuation ratios, short interest, address and number of employees for Pacific Ethanol Inc. (PEIX)
Hi, Ive been reading about using Ethanol for declotting lines with lipids. Is anyone doing this out there and where do you get the ethanol? Thanks
One ethanol producer aims to enter the IPO market next week, and another is planning to later this year, despite mediocre trading from two other ethanol stocks that made their debuts this summer.
Domestic ethanol stocks posted the first draw in three weeks as blending demand continued higher during the third week of November, reaching the highest level since late October.
In previous work, we identified genetic correlations between cAMP accumulation in the cerebellum and sensitivity to the incoordinating effects of ethanol. A genetic correlation suggests that common genes underlie the phenotypes investigated. One method for provisionally identifying genes involved in a given phenotypic measure is quantitative trait locus (QTL) analysis. Using a panel of 30 BXD recombinant inbred strains of mice and the progenitors (DBA/2J and C57BL/6J), and the dowel test for ataxia, we measured the blood ethanol concentrations at the time an animal first fell from the dowel and acute functional tolerance (AFT), and investigated cAMP signaling in the cerebellum. Cyclic AMP accumulation was measured in whole-cell preparations of cerebellar minces from individual mice under basal or stimulated conditions. We conducted a genome-wide QTL analysis of the behavioral and biochemical measures with >2000 genetic markers to identify significant associations. Western blot and comparative ...
Separately, chronic alcohol ingestion and HIV-1 infection are associated with severe skeletal muscle derangements, including atrophy and wasting, weakness, and fatigue. One prospective cohort study reported that 41% of HIV-infected patients met the criteria for alcoholism, however; few reports exist on the co-morbid effects of these two disease processes on skeletal muscle homeostasis. Thus, we analyzed the atrophic effects of chronic alcohol ingestion in HIV-1 transgenic rats and identified alterations to several catabolic and anabolic factors. Relative plantaris mass, total protein content, and fiber cross-sectional area were reduced in each experimental group compared to healthy, control-fed rats. Alcohol abuse further reduced plantaris fiber area in HIV-1 transgenic rats. Consistent with previous reports, gene levels of myostatin and its receptor activin IIB were not increased in HIV-1 transgenic rat muscle. However, myostatin and activin IIB were induced in healthy and HIV-1 transgenic rats fed
TY - JOUR. T1 - Responses of cerebral arterioles during chronic ethanol exposure. AU - Mayhan, William. PY - 1992. Y1 - 1992. N2 - The purpose of this study was to examine the effects of ethanol exposure on responses of cerebral arterioles in vivo. Rats were fed liquid diets with or without ethanol for 2-3 mo. Using intravital microscopy, we measured diameter of cerebral arterioles in non-ethanol- and ethanol-fed rats in response to acetylcholine, histamine, ADP, the thromboxane analogue (U- 46619), and nitroglycerin. In non-ethanol-fed rats, acetylcholine, histamine, and ADP produced dose-related dilatation of cerebral arterioles. In ethanol- fed rats, however, acetylcholine produced vasoconstriction, and vasodilatation in response to histamine and ADP was impaired. Dilatation of cerebral arterioles in response to nitroglycerin and vasoconstriction in response to the thromboxane analogue (U-46619) were similar in non-ethanol- fed and ethanol-fed rats. Thus these findings suggest that chronic ...
Chronic alcoholics who also binge drink (i.e., acute on chronic) are prone to an exacerbated liver injury but its mechanism is not understood. We therefore investigated the in vivo effects of chronic and binge ethanol ingestion and compared to chronic ethanol followed by three repeat binge ethanol on the liver of male C57/BL6 mice fed ethanol in liquid diet (4%) for four weeks followed by binge ethanol (intragastric administration, 3.5 g/kg body weight, three doses, 12h apart). Chronic followed by binge ethanol exacerbated fat accumulation, necrosis, decrease in hepatic SAM and SAM:SAH ratio, increase in adenosine levels, and elevated CYP2E1 levels. Histone H3 lysine acetylation (H3AcK9), dually modified phosphoacetylated histone H3 (H3AcK9/PS10), and phosphorylated H2AX increased after binge whereas phosphorylation of histone H3 ser 10 (H3S10) and H3 ser 28 (H3S28) increased after chronic ethanol-binge. Histone H3 lysine 4 and 9 dimethylation increased with a marked dimethylation in H3K9 in chronic
Evidence that brain edema and aquaporin-4 (AQP4) water channels have roles in experimental binge ethanol-induced neurodegeneration has stimulated interest in swelling/edema-linked neuroinflammatory pathways leading to oxidative stress. We report here that neurotoxic binge ethanol exposure produces comparable significant effects in vivo and in vitro on adult rat brain levels of AQP4 as well as neuroinflammation-linked enzymes: key phospholipase A2 (PLA2) family members and poly (ADP-ribose) polymerase-1 (PARP-1). In adult male rats, repetitive ethanol intoxication (3 gavages/d for 4 d, ∼9 g/kg/d, achieving blood ethanol levels ∼375 mg/dl;
The liver plays a key role in the metabolism of alcohol and is also sensitive to the deleterious effects of chronic alcohol consumption. In humans, chronic alcohol consumption leads to a characteristic set of changes to the metabolism of lipids in the liver that is referred to as an "alcoholic fatty liver". In humans, AFL is characterized by an increase in liver weight, accumulation of triglyceride and changes in the expression of genes involved in lipid metabolism. In severe cases, these metabolic changes result in the enlargement and fibrillization of the liver and are considered risk factors for cirrhosis and liver cancer.. Previous work suggests that there may be links between mutations in the circadian system and liver metabolism. The transcription of many genes in liver, including those involved in lipid metabolism, is regulated on the circadian time scale [8, 22]. Furthermore, mice with mutations in core elements of the circadian timing system also exhibit deficits in liver function. In ...
Increasing evidence suggests that ethanol-induced changes in cyclic AMP (cAMP) signal transduction play a critical role in the acute and chronic effects of ethanol. Here we have investigated the effects of ethanol on cAMP signal transduction in primary cultures of rat hepatocytes. Acute exposure to ethanol had a biphasic effect on glucagon-receptor-dependent cAMP production in intact cells: 25-50 mM-ethanol decreased cAMP, whereas treatment with 100-200 mM-ethanol increased cAMP. After chronic exposure to 50-200 mM-ethanol for 48 h in culture, glucagon-receptor-dependent cAMP levels were increased, but no change in glucagon receptor number was observed. These effects of ethanol were independent of ethanol oxidation. Chronic ethanol treatment also increased adenosine-receptor- and forskolin-stimulated cAMP production. Increased cAMP production was also observed upon stimulation of adenylate cyclase with glucagon, forskolin and F- in membranes isolated from cells cultured with 100 mM-ethanol for ...
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THE POTENTIATING ACTION OF HYDROXYZINE MUST BE CONSIDERED WHEN THE DRUG IS USED IN CONJUNCTION WITH CENTRAL NERVOUS SYSTEM DEPRESSANTS SUCH AS NARCOTICS, NON-NARCOTIC ANALGESICS AND BARBITURATES. Therefore when central nervous system depressants are administered concomitantly with hydroxyzine their dosage should be reduced.. Since drowsiness may occur with use of this drug, patients should be warned of this possibility and cautioned against driving a car or operating dangerous machinery while taking Atarax. Patients should be advised against the simultaneous use of other CNS depressant drugs, and cautioned that the effect of alcohol may be increased.. ...
The present study sought to examine the effects of chronic ethanol exposure and withdrawal on glutamate release probability at inputs arising from two subdivisions of the medial prefrontal cortex to the basolateral amygdala. We used a combination of optogenetics and chemogenetics to document the neurophysiological and behavioral alterations of dmPFC and vmPFC terminals in the BLA. The major findings of the study are that withdrawal from chronic ethanol exposure increases optogenetically stimulated glutamate release from dmPFC-BLA terminals but decreases the glutamate release from vmPFC terminals. Additionally, we demonstrate that chemogenetic inhibition of dmPFC terminals in the BLA reduces withdrawal-induced anxiety-like behavior. And finally, we show that local feedback-like GABAergic circuits make significant contributions to optically gated responses from both dmPFC and vmPFC terminals. Together, these data provide the first characterization of how chronic ethanol exposure and withdrawal ...
Introduction. How does caffeine and ethanol affect the heart rate? Introduction At rest a normal adult heart beats around 75 times per minute. During strenuous exercise it may rise to 200 beats per minute. The SAN (sino-atrial node) controls the heart rate. Information is sent via two autonomic nerves that link the SAN with cardiovascular centre in the medulla of the brain, the rate increases or decreases depending on the information received. Factors, which affect the heart: , The secretion of adrenaline. This may be under stress, excitement or other emotions. , Movement of the limbs (exercise). Heart rate and breathing rate increase due to oxygen levels falling and levels of carbon dioxide rising. , Blood pressure. When blood pressure is too high, a mechanism prevents increase in heart rate. Adrenaline is a hormone, which is produced by the adrenal gland; it is usually secreted in tiny amounts, when stressed or scared. It raises your heart rate immediately. Adrenaline improves the strength of ...
Intake of ethanol by rats, at a dose of 10 to 12 g/kg daily for two weeks, led to a slower onset and shorter duration of pentobarbital-induced sleep (30 mg/kg i.p.) than in pair-fed controls with isocaloric substitution of sucrose for ethanol. The pentobarbital concentrations in both plasma and brain were significantly lower in ethanol-treated animals at 15 minutes after injection, but not at 30 to 60 minutes. During the latter times, the rate of disappearance of pentobarbital from plasma did not differ in the two groups. The rate of metabolism of pentobarbital by liver slices in vitro was 33% lower for the chronic ethanol group than the controls. In contrast, pretreatment with phenobarbital for one week led to a significant increase in the rate of pentobarbital metabolism by liver slices. It is concluded that the changes in pentobarbital sleeping time after chronic ethanol treatment are primarily the result of changes in sensitivity of the nervous system, rather than of changes in distribution ...
The IL-10 promoter is regulated through the p38 MAPK pathway in human macrophages (40). Our results demonstrated that acute ethanol treatment increased the levels of phosphorylated p38 in the same LPS-stimulated human monocytes that showed increased IL-10 and reduced TNF-α production. These effects of acute ethanol in our experiments were similar to the effects of CO, a product of HO-1 activation on monocytes (13). Consistent with the previously described role of p38 MAPK activation in IL-10 induction, inhibition of p38 activity with SB203580 prevented ethanol-induced augmentation of monocyte IL-10 production (28, 40). Activation of p38 MAPK has been shown to induce HO-1 expression in various cell types including macrophages (13), hepatocytes (24), pulmonary epithelial cells (41), and vascular cells (42). Our studies revealed that augmentation of p38 MAPK phosphorylation contributed to alcohol-induced HO-1 activation in LPS-stimulated monocytes. Recent studies demonstrated that transcriptional ...
BACKGROUND: The NMDA receptor represents a particularly important site of ethanol action in the CNS. We recently reported that NMDA receptor 2B (NR2B) gene expression was persistently up-regulated following chronic intermittent ethanol (CIE) treatment. Increasing evidence that epigenetic mechanisms are involved in dynamic and long-lasting regulation of gene expression in multiple neuroadaptive processes prompted us to investigate the role of DNA methylation in mediating CIE-induced up-regulation of NR2B gene transcription. To dissect the changes of DNA methylation in the NR2B gene, we have screened a large number of CpG sites within its 5-regulatory area following CIE treatment. METHODS: Primary cortical cultured neurons were subjected to ethanol treatment in a CIE paradigm. Bisulfite conversion followed by pyrosequencing was used for quantitative measurement and analysis of CpG methylation status within the 5-regulatory area of the NR2B gene; chromatin immunoprecipitation (ChIP) assay was ...
Administration of topical antibiotics led to resolution of the lesions within 3 weeks, and there were no signs of scarring or recurrence.. The clinical presentation and histopathologic findings were consistent with a diagnosis of coma blisters.. Clinically, coma blisters are characterized by tense clear or hemorrhagic blisters that develop on erythematous-violaceous macules or plaques of varying size. The lesions typically appear within 24hours of the intake of drugs and within 48 to 72hours of the loss of consciousness. They primarily develop on pressure points, such as fingers and toes, elbows, knees, ankles, and heels. They are self-limiting and heal within days or weeks, without causing scarring or atrophy. The only treatment indicated thus is topical treatment to prevent secondary infections.2,8. Multiple factors have been implicated in the etiology and pathogenesis of coma blisters, including local pressure or friction, generalized hypoxia and tissue ischemia, direct toxicity due to drugs ...
2Research Center for Alcoholic Liver Disease and Pancreatitis and Cirrhosis, School of Medicine, University of Southern California, Los Angeles, USA. In the search for novel targets for chronic alcohol-induced inflammatory responses, we recently started exploring the therapeutic potential of ATP-gated purinergic P2X7 receptors (P2X7Rs). Despite the recognized important role in several neurodegenerative pathologies and inflammatory conditions, the role of P2X7Rs in ethanol-induced inflammation and organ damage is still unknown. Using a chronic ethanol exposure model of alcohol liver disease that combines intragastric (iG) ethanol feeding and high fat diet (Hybrid) in C57BL/6J mice, our recent work demonstrated an increased expression of P2X7Rs that paralleled neuroinflammatory changes in several ethanol-sensitive brain regions. These findings served the basis for the hypothesis that there is a functional link between P2X7Rs and chronic ethanol-induced inflammatory response leading to organ ...
the precise molecular sites and mechanisms of action for ethanol in ligand-gated ion channels (LGICs) in general, and in GlyRs and GABAARs specifically, are just now starting to become understood. The present dissertation focuses on studies we conducted that address this issue using molecular biology, pressure antagonism, electrophysiology and molecular modeling strategies to probe, identify and model the initial molecular sites and mechanisms of ethanol action in GlyRs and GABAARs. Specifically, this work focuses on the Loop 2 region in the extracellular domain of GlyRs and GABAARs and (1) Provides evidence that position 52 in Loop 2 is a target for ethanol action and antagonism in GlyRs; (2) Demonstrates that the structural bases for the actions of ethanol and pressure on this common target are different and (3) Provides strong evidence that the structure of Loop 2 in GlyRs, GABAARs and possibly across LGICs may be a key factor in controlling the sensitivity of these receptors to ethanol. ...
Ethanols effects on lipid metabolism and membrane lipid composition; membrane protein-lipid interactions; production and isolation of fatty acid ethyl esters and their pathological effects; the effect of ethanol on metastatic and nonmetastatic breast cancer cells. ...
Ethanol, oil and livestock groups all weighed in with opinions on the Renewable Fuels Standard (RFS) last week as Congress returned to work.
The neurochemical mechanisms that regulate development of alcohol use disorder (AUD) are complex, and gut-brain peptides were recently pinpointed as novel modulators. Gut-brain peptides, such as glucagon-like peptide-1 (GLP-1), are well known for their ability to regulate food intake and appetite. GLP-1 also controls glucose homeostasis, which lead to the approval of GLP-1 receptor agonists for treatment of diabetes type II. These pharmacotherapies, including exenatide/exendin-4(Ex4) and liraglutide, have also been tested in various animal modes of AUD. In mice, Ex4 attenuates the acute behavioural responses to alcohol. Rat studies additionally show that Ex4 reduces the intake and the intravenous operant self-administration of alcohol and decreases the motivation to consume alcohol. Further studies established that Ex4 modulates alcohol-mediated behaviours via activation of GLP-1 receptors in reward related areas and an area of the hindbrain. In rodents, liraglutide reduces withdrawal symptoms ...
Looking for a cure for fatty liver?: Does Alcohol Causes Fatty Liver. The Fatty Liver Site, Tips and natural treatments for fatty liver.
Red wine is composed of more than 500 compounds although only a few are present at concentrations of more than 100 mg/L. These include water, glycerol, ethanol, sugar and organic acids. There is increasing evidence supporting the cardioprotective effects of ethanol (Figure 2), although the mechanisms of cardioprotection remain somewhat obscure. Ethanol decreases sympathetic activity, thereby decreasing heart rate and cardiac contraction while inducing coronary vasodilation; all these effects lead to cardioprotection. On the other hand, Grassi et al (50) showed that increased plasma ethanol level significantly elevates the blood pressure, heart rate and sympathetic nerve activity. Low to moderate concentrations of ethanol are shown to inhibit coronary muscle contraction, increase coronary flow and improve the cardiac output (51). The mechanisms by which ethanol is a vasodilator are still unknown, however, a study on the effects of changes in extracellular Ca2+ on muscle contractions supports a ...
Grown in nearly every country, then sent for fermentation by using glucose produced from sugar from the hydrolysis of starch, in the presence of yeast and temperature of less than 37°C to produce ethanol. For instance the conversion of invertase to glucose and fructose or the conversion of glucose to zymase and ethanol. By direct hydration using ethylene (ethylene hydration) or other alkenes from cracking of fractions of distilled crude oil. Ethanol in alcoholic beverages has been consumed by humans since prehistoric times for a variety of hygienic, dietary, medicinal, religious, and recreational reasons. The consumption of large doses of ethanol causes drunkenness (intoxication), which may lead to a hangover as its effects wear off. Depending upon the dose and the regularity of its consumption, ethanol can cause acute respiratory failure or death. Because ethanol impairs judgment in humans, it can be a catalyst for reckless or irresponsible behavior. The LD50 of ethanol in rats is 10.3 g/kg. ...
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This investigation assesses the role of poly(ADP-ribose) polymerase in ethanol-mediated hepatotoxicity using the untransfected HepG2 hepatocellular carcinoma line, an established, well-characterized toxicological model. HepG2 cells were treated with ethanol at concentrations between 100 mM and 800 mM, and assessed for markers of cytotoxicity. PARP-1 activity in total cell protein lysates was quantified as a proxy of apoptotic induction at six hours. Our results demonstrated a 1.43-fold AST activity increase in culture medium isolates of cells exposed to 800 mM without significant effect on cellular viability. PARP-1 activity varied greatly and results for enzyme activity remained inconclusive. The results suggest a high degree of insensitivity to ethanol toxicity and nuclear enzyme activity, demonstrating the metabolic irrelevance of untransfected HepG2 in ethanol toxicosis. There is a need to characterize phase 1 metabolic enzyme expression profiles relevant to ethanol for CYP2E1 and ADH pathways to
Alcohol produces injury to cells by dehydration and precipitation of the cytoplasm or protoplasm. This accounts for its bacteriocidal and antifungal action. When alcohol is injected in close proximity to nerve tissues, it produces neuritis and nerve degeneration (neurolysis). Ninety to 98% of ethanol that enters the body is completely oxidized. Ethanol is also used as a cosolvent to dissolve many insoluble drugs and to serve as a mild sedative in some medicinal formulations ...
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NIH Funding Opportunities and Notices in the NIH Guide for Grants and Contracts: Mechanisms of Alcohol-associated Cancers (R21) PA-12-147. NIAAA
NIH Funding Opportunities and Notices in the NIH Guide for Grants and Contracts: Mechanisms of Alcohol-associated Cancers (R01) PA-12-146. NIAAA
️⭐️⭐️⭐️⭐️ ativan length of time in system It solves the problem for you quickly How Long Does Xanax Stay In Your System? What what class of drug is glucophage You are Looking Best pill? How long do drugs stay in your system ? Check More ». ★ length of time ativan stays in system. - Xanax (Alprazolam) The length of time do you assume Xanax (and also its metabolites) remained in your system? The length of time Xanax stays in the system varies from person to person. Stop wasting your time with unanswered searches. How Long Do Xanax Withdrawals Last As a central nervous system depressant, Xanax age at first use, genetics, and length of time using or abusing Xanax. Length of time xanax in system. How Long Does Xanax factors that might influence how long Xanax stays in your system, The total length of time youve been taking Xanax will also affect how. The length of time any illicit or prescribed drugs stay in your system will vary Best xanax length of time in system Sale ativan ...
According to the US Department of Health and Human Services, "Opioids (such as the pain relievers OxyContin and Vicodin), central nervous system depressants (e.g., Xanax, Valium), and stimulants (e.g., Ritalin, Adderall) are the most commonly abused prescription drugs ...
Chronic alcohol exposure affects the central nervous system, influences behavior, and induces neuroadaptive changes in vertebrate species including our own. literature to be alcohol related. We conclude that the zebrafish is an excellent tool for the analysis of genes associated with alcohols actions in vertebrates, one which may facilitate the discovery and better understanding of […]. ...
M. R. Moore, A. D. Beattie, G. Thompson, A. Goldberg; Negative Correlation of Blood Ethanol and Erythrocyte Delta-Aminolaevulic Acid (ALA) Dehydrase Levels in Man. Clin Sci 1 May 1970; 38 (5): 33P. doi: https://doi.org/10.1042/cs038033Pb. Download citation file:. ...
billions of dollars have been spent on making transportation environmentally friendly and sustainable through the use of ethanol. Despite the magnitude of..
Im not sure of the context of your question. In general, there are two ways that a small molecule like ethanol (or glycerol or a sugar) can get across a membrane. There can either be a transport protein that mediates passage across the membrane or the substance can diffuse across. Ethanol can do both. It is not a charged molecule and its small, so it can diffuse across the membrane. That means it is dissolved in the water outside the cell, then dissolves in the lipid of the membrane when it contacts the membrane through random motion. Once in the membrane it will diffuse through the membrane by random motion and eventually dissolve itself back into the water. Its random which side of the membrane it exits. So if it enter from outside, it doesnt necessarily end up inside, its roughly 50:50 whether it ends inside or outside. Some but not all cells have a protein that can transport ethanol. It would have a binding site for ethanol. Once bound, the ethanol will cause the protein/transporter to ...
Methanol and ethanol are variants of alcohol, and they have different properties and uses. Methanol is a poisonous chemical derived through synthetic processes, while commercial ethanol is produced by factory fermentation of food crops. Both substances can be used as energy sources, but methanol serves mainly as a ...
Seth/Chad: How can you not like an episode of Lost that includes James drinking himself to the point of acute ethanol toxicity while listening to the l ...
In the midst of rising oil prices, the economics of producing cellulosic ethanol are becoming increasingly favorable and several companies are steadfastly moving to commercialize various process technologies. It would be easy to view this development as a race pitting one technology against the other but is that really the case? Is one approach better than another?
Ethanol is not the energy panacea that environmentalists would have you believe. The production of ethanol has a number of unintended consequences and ethanol can never completely replace gasoline.
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My supply of Iso-Propyl Alcohol has ran out, and I need something as a fuel and disinfectant for random experiments I do all the time, and Im not...
FROM THE JULY ISSUE: RFA caps corn ethanol at 15 billion gallons per year and we have reached and exceeded that level. Future growth must meet true demand, and that demand is blocked by unnecessary, arbitrary and baseless regulations.
A pair of ultra-micro cells enables easy and reproducible analysis of very small sample volumes, down to 30 µL, and the reference material set provides validation of the ordinate and wavelength accuracy of your Lambda 25. The liquid sipper enables fast, in-situ liquid sampling directly from the container. For use with the LAMBDA UV/Vis Systems. ...
Market Outlook: U.S. ethanol prices are softer this week as rising stocks and lighter demand pressure the market. Nearby CBOT ethanol futures have continued to move lower following last weeks WASDE report from USDA, despite lower corn futures prices. Nearby ethanol futures are down 0.71 cents/liter (2.7 cents/gallon) from last week, priced at 33.5 cents/liter (126.8 cents/gallon). Midwest rack prices are similarly lower, falling 3.7 percent to 37.28 cents/liter (141.13 cents/gallon) as cash market trading remains quiet amid growing supplies.
The ethanol industry produces more ethanol than the US fuel market can readily use. The industry has been lobbying to allow the year-round sales of E15.
The more popular ethanol has become, the more it rides the nations rails. An estimated 70 percent of ethanol produced in the U.S. is delivered by railroad, said Kristy Moore, technical director of the Renewable Fuels Association.
If you are buying an ethanol fireplace or are thinking of buying one check out the ethanol fireplaces facts before you buy. There is much hype and truth on
Sugaronline is an independent website including sugar and ethanol news, prices and reports for a global sugar and ethanol industries
Ethanol investments are so volatile due to a number of factors, including the fact that the industry that creates ethanol from...
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The latest weekly supply report from the U.S. Energy Information Administration shows domestic ethanol supply declined for the second straight week.
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This report is a comprehensive research of ethanol market in United States. The report starts with giving brief country profile for United States, including
Combining Ammonia and Ethanol in a single RIQAS programme, participants can consolidate their EQA requirements whilst reducing costs.
The ethanol debate sometimes seems like Field of Dreams. It's the same today that it was ten years ago and there's lots of ...
Billions of dollars are being spent on new technologies and industries dealing with the advent of ethanol as an energy source for the U.S.
Findings show that American Indians are at much greater risk than other ethnic groups.. In 2009, according to the Centers for Disease Control and Prevention, suicide ranked as the 10th leading overall cause of death in the United States. Prior research has also shown that alcohol use disorders confer increased risk for suicide, and are second only to mood disorders as common among individuals who have committed suicide. A study of the prevalence and sociodemographic correlates of suicide involving acute alcohol intoxication among U.S. ethnic minorities has found that American Indians are at much greater risk than other groups.. Results will be published in the May 2013 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.. "I do not think that most people in the U.S. are aware that suicide is ranked as the 10th leading cause of death," said Raul Caetano, regional dean (Dallas) and professor of epidemiology at The University of Texas School of Public ...
Inositol phosphate accumulation and adenylate cyclase activity were investigated in the cortex of young and aged ethanol-treated rats. Three months of ethanol treatment of young rats decreased maximal stimulation of inositol phosphate accumulation by carbachol by 26%, from 494 ± 76% of basal turnover in control animals to 396 ± 54% in ethanol-treated animals (mean ± SD). In aged rats ethanol-related changes were no longer observed but age-related changes were evident. EC50 was significantly higher than in young animals and maximal stimulation was significantly lower. Basal adenylate cyclase activity in cortical membranes of all groups of animals was not different. Forskolin-stimulated adenylate cyclase activity was not affected by ethanol treatment, but was higher in aged animals. The activity of forskolin-stimulated adenylate cyclase in the presence of carbachol was higher in both young and aged ethanol-treated animals, when compared to young controls. These results suggest that both ethanol ...
Fetal alcohol spectrum disorder (FASD) is a leading form of neurodevelopmental delay in Canada, affecting an estimated 3000 babies per year. FASD involves a range of disabilities that entail significant costs to affected individuals, families, and society. Exposure to alcohol in utero is a necessary factor for FASD development, and this has led to FASD being described as "completely preventable". However, there are significant ethical challenges associated with FASD prevention. These challenges revolve around 1) what should be communicated about the risks of alcohol consumption during pregnancy, given some ongoing scientific uncertainty about the effects of prenatal alcohol exposure, and 2) how to communicate these risks, given the potential for stigma against women who give birth to children with FASD as well as against children and adults with FASD ...
Background: In Fetal Alcohol Spectrum Disorder (FASD), structural and functional abnormalities in the cerebellum persist through adolescence and beyond. We hypothesize th..
TY - JOUR. T1 - Liver Injury, Endotoxemia, and Their Relationship to Intestinal Microbiota Composition in Alcohol-Preferring Rats. AU - Posteraro, Brunella. AU - Paroni Sterbini, Francesco. AU - Petito, Valentina. AU - Rocca, Stefano. AU - Cubeddu, Tiziana. AU - Graziani, Cristina. AU - Arena, Vincenzo. AU - Vassallo, Gabriele A.. AU - Mosoni, Carolina. AU - Lopetuso, Loris. AU - Lorrai, Irene. AU - Maccioni, Paola. AU - Masucci, Luca. AU - Martini, Cecilia. AU - Gasbarrini, Antonio. AU - Sanguinetti, Maurizio. AU - Colombo, Giancarlo. AU - Addolorato, Giovanni. PY - 2018/12/1. Y1 - 2018/12/1. N2 - Background: There is strong evidence that alcoholism leads to dysbiosis in both humans and animals. However, it is unclear how changes in the intestinal microbiota (IM) relate to ethanol (EtOH)-induced disruption of gut-liver homeostasis. We investigated this issue using selectively bred Sardinian alcohol-preferring (sP) rats, a validated animal model of excessive EtOH consumption. Methods: ...
Adiponectin, an adipokine predominantly secreted from adipocytes, has been shown to play protective roles against chronic alcohol consumption. While excessive ROS production in macrophages is considered one of the critical events for ethanol-induced damage in various target tissues, the effect of adiponectin on ethanol-induced ROS production is not clearly understood. In the present study, we investigated the effect of globular adiponectin (gAcrp) on ethanol-induced ROS production and the potential mechanisms underlying these effects of gAcrp in macrophages. Here, we demonstrated that gAcrp prevented ethanol-induced ROS production both in RAW 264.7 macrophages and primary murine peritoneal macrophages. Globular adiponectin also inhibited ethanol-induced activation of NADPH oxidase. In addition, gAcrp suppressed ethanol-induced increase in expression of NADPH oxidase subunits, including Nox2 and p22phox, via modulation of NF-κB pathway. Furthermore, pretreatment with Compound C, a selective ...
Title:Analgesic and CNS Depressant Activities of Sea Anemone Heteractis aurora Nematocyst Toxin. VOLUME: 16 ISSUE: 3. Author(s):Sengapillai Thangaraj, Subramanian Bragadeeswaran, Natarajah Srikumaran and Anbukkarasu Suguna. Affiliation:Marine Biotoxinology Lab. Centre of Advanced Study in Marine Biology, Faculty of Marine Sciences, Annamalai University, Parangipettai - 608 502, Tamil Nadu, India.. Keywords:Analgesic activity, CNS depressant activity, Heteractis aurora, Haemolytic activity, Sea anemone.. Abstract:Marine organisms are the excellent sources for biologically active compounds. Cnidarian venoms are potentially valuable materials used for biomedical research and drug development. The present work was carried out to analyse haemolytic, analgesic and CNS depressant activity of sea anemone Heteractis aurora. In haemolytic assay, among the five different RBC blood cells, the chicken blood exhibited maximum hemolytic activity of 64 Hemolytic Unit (HU). The maximum Analgesic Ratio (AR) of 5 ...
Fetal alcohol spectrum disorders (FASDs) are a group of conditions that can occur in a person whose mother drank alcohol during pregnancy. Problems may include an abnormal appearance, short height, low body weight, small head size, poor coordination, low intelligence, behavior problems, and problems with hearing or seeing. Those affected are more likely to have trouble in school, legal problems, participate in high-risk behaviors, and have trouble with alcohol or other drugs. The most severe form of the condition is known as fetal alcohol syndrome (FAS). Other types include partial fetal alcohol syndrome (pFAS), alcohol-related neurodevelopmental disorder (ARND) and alcohol-related birth defects (ARBD). Some accept only FAS as a diagnosis, seeing the evidence as inconclusive with respect to other types. Fetal alcohol spectrum disorders are caused by drinking alcohol during pregnancy. Surveys from the United States have found about 10% of pregnant women have drunk alcohol in the last month, and ...
The lack of universally accepted diagnostic criteria and the high rate of psychiatric comorbidity make it difficult to diagnose Fetal Alcohol Spectrum Disorder (FASD). In an effort to improve the diagnosis of FASD, the current study aimed to identify a neurodevelopmental profile that is both sensitive and specific to FASD. A secondary analysis was conducted on data obtained from the Canadian component of the World Health Organization International Study on the Prevalence of FASD. Data on neurodevelopmental status and behavior were derived from a battery of standardized tests and the Child Behavior Checklist for 21 children with FASD, 28 children with other neurodevelopmental disorders, and 37 typically developing control children, aged 7 to 11 years. Two latent profile analyses were performed to derive discriminative profiles: i) children with FASD compared with typically developing control children, and ii) children with FASD compared with typically developing control children and children with other
The National Institute on Alcohol Abuse and Alcoholism (NIAAA)-part of the National Institutes of Health, the Nations medical research agency-has a large research program on fetal alcohol spectrum disorders (FASD) that sponsors projects on preventing prenatal alcohol exposure, treating women with alcohol use disorder, improving the diagnosis of FASD, establishing more precise
TY - JOUR. T1 - Dopamine Activity in the Nucleus Accumbens During Consummatory Phases of Oral Ethanol Self-Administration. AU - Doyon, William M.. AU - York, Jennifer L.. AU - Diaz, Laurea M.. AU - Samson, Herman H.. AU - Czachowski, Cristine L.. AU - Gonzales, Rueben A.. PY - 2003/10. Y1 - 2003/10. N2 - Background: This present study was designed to clarify the role of dopamine in the nucleus accumbens during operant ethanol self-administration by separating bar pressing (ethanol seeking) from ethanol consumption. Furthermore, we sought to define the relationship between ethanol in the brain and the accumbal dopamine response after oral self-administration of ethanol. Methods: Two separate groups of male Long-Evans rats were trained to bar press with 10% ethanol or water. Rats were trained to elicit an escalating number of bar presses across daily sessions before gaining access to the drinking solution for 20 min. Microdialysis was performed before (during a waiting period), during, and after ...
The effect of long-term ethanol exposure on muscarinic receptors was investigated in human neuroblastoma SH-SY5Y cells. Exposure to 100 mM ethanol for 4 days enhanced both peak and steady-state levels of carbachol-stimulated inositol 1,4,5-bisphosphate increase. An ethanol concentration of 50 mM was sufficient for an enhancement of this event. The carbachol-stimulated decrease in [3H]inositol-labeled [3H]phosphatidylnositol 4,5-bisphosphate and increase [3H]inositol trisphosphate and [3H]inositol bisphosphate were also potentiated in ethanol-treated cells, which demonstrated that the receptor-stimulated activation of phospholipase C is augmented. Experiments with pirenzepine showed that carbachol-stimulated inositol 1,4,5-trisphosphate increase is mediated via M1 receptors both in ethanol-treated and control cells. Ethanol exposure for 2 or 4 days also caused an increase in [3H]N-methylscopolamine and [3H]quinuclidinyl benzilate binding sites and elevation of [3H]pirenzepine binding, which ...

Alcohol and Substance Abuse Central Nervous System DepressantsAlcohol and Substance Abuse Central Nervous System Depressants

... ... nervous system damage, inflammation of the pancreas, heart disease, high blood pressure, stroke. ... If too much alcohol is taken into the body at once, the depressant effects of the drug will cause the heart and lungs to stop ...
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Perspectives in Drug Discovery : Central Nervous System DepressantsPerspectives in Drug Discovery : Central Nervous System Depressants

Perspectives in Drug Discovery: Central Nervous System Depressants. Jones, Alan Wayne Linköping University, Department of ...
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Definition of central nervous system depressant - NCI Dictionary of Cancer Terms - National Cancer InstituteDefinition of central nervous system depressant - NCI Dictionary of Cancer Terms - National Cancer Institute

Central nervous system depressants are used to treat insomnia (trouble sleeping), anxiety, panic attacks, and seizures. ... Examples of central nervous system depressants are benzodiazepines, barbiturates, and certain sleep medicines. Central nervous ... central nervous system depressant listen (SEN-trul NER-vus SIS-tem dee-PREH-sunt) A type of drug that slows down brain activity ... Central nervous system depressants are used to treat insomnia (trouble sleeping), anxiety, panic attacks, and seizures. They ...
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Central Nervous System Depressants - Why They Are Leading to Serious AddictionCentral Nervous System Depressants - Why They Are Leading to Serious Addiction

Central Nervous System depressants are a group of drugs that depress the nervous system like sedatives and barbiturates. ... What Are Central Nervous System Depressants (CNS)?. CNS depressants (Central Nervous System depressants) are medications that ... Treatment for CNS Depressant Addiction. It is possible to overcome an addiction to Central Nervous System depressants, but ... Once the person becomes addicted, he or she will crave Central Nervous System depressants and seek the drugs in spite of any ...
more infohttp://www.4rehabilitation.com/cns-depressants-why-they-are-leading-to-serious-addiction/

Bioactive Polyphenols from the Methanol Extract of Cnicus arvensis (L.) Roth Demonstrated Antinociceptive and Central Nervous...Bioactive Polyphenols from the Methanol Extract of Cnicus arvensis (L.) Roth Demonstrated Antinociceptive and Central Nervous...

Roth Demonstrated Antinociceptive and Central Nervous System Depressant Activities in Mice. Mahmudur Rahman,1 Amina Khatun,2 ... In open field test for CNS depressant activity, the extract showed depression of locomotor activity for 150 and 300 mg/kg body ... The identified polyphenols are reputed for antinociceptive and CNS depressant activity. The present findings support the use of ...
more infohttps://www.hindawi.com/journals/ecam/2015/794729/abs/

SciELO - Public Health - The effect of central nervous system depressant, stimulant and hallucinogenic drugs on injury severity...SciELO - Public Health - The effect of central nervous system depressant, stimulant and hallucinogenic drugs on injury severity...

The effect of central nervous system depressant, stimulant and hallucinogenic drugs on injury severity in patients admitted for ... The effect of central nervous system depressant, stimulant and hallucinogenic drugs on injury severity in patients admitted for ... Pooled data analyses in previous studies that grouped substances with opposite effects on the central nervous system (CNS) may ... For example, drugs with different effects, including opposite effects, on the central nervous system (CNS) are usually pooled ...
more infohttps://scielosp.org/article/gs/2019.v33n1/4-9/en/

Central Nervous System Depressants | CTDCentral Nervous System Depressants | CTD

Central Nervous System Depressants 2.. Chemicals ← Chemical Actions and Uses ← Pharmacologic Actions ← Therapeutic Uses ← ... Central Nervous System Agents ← Central Nervous System Depressants Top ↑ Descendants Central Nervous System Depressants ... A very loosely defined group of drugs that tend to reduce the activity of the central nervous system. The major groups included ... Central Nervous System Depressants Equivalent Terms CNS Depressants , Depressants, CNS Definition ...
more infohttp://ctdbase.org/detail.go?type=chem&acc=D002492

Coma Blisters After an Overdose of Central Nervous System Depressants | Actas Dermo-Sifiliográficas (English Edition)Coma Blisters After an Overdose of Central Nervous System Depressants | Actas Dermo-Sifiliográficas (English Edition)

Coma Blisters After an Overdose of Central Nervous System Depressants Ampollas del coma tras sobredosis de fármacos depresores ... Coma blisters after poisoning caused by central nervous system depressants: Case report including histopathological findings ... Since then, it has been mainly associated with overdose of drugs and nervous system depressants, such as barbiturates, ... Ampollas del coma tras sobredosis de fármacos depresores del sistema nervioso central. Actas Dermosifiliogr. 2017;108:81-83. ...
more infohttp://actasdermo.org/en/coma-blisters-after-an-overdose/articulo/S157821901630302X/

Drug and Alcohol Abuse Prevention Program | AdministrationDrug and Alcohol Abuse Prevention Program | Administration

Depressants (of the central nervous system). *Opioid derivatives/narcotics (heroin, morphine, codeine, hydrocodone [Lortab or ... Gamma Hydroxy Butrate (GHB) is a synthetic "date rape drug" that is a colorless and odorless central nervous system depressant ... Permanent damage to lungs, brain, liver, and immune system may occur.. Stimulants. * *Amphetamines (uppers, speed), ... They are especially dangerous when mixed with other depressants such as alcohol.. Rohypnol (flunitrazepam) is also a ...
more infohttp://www.auburn.edu/administration/campus-safety/prevention.html

Azelastine - FDA prescribing information, side effects and usesAzelastine - FDA prescribing information, side effects and uses

... central nervous system depressants should be avoided because reductions in alertness and impairment of central nervous system ... central nervous system depressants because additional reductions in alertness and additional impairment of central nervous ... Central Nervous System Depressants. Concurrent use of Azelastine hydrochloride nasal solution (nasal spray), 0.1% with alcohol ... Concurrent Use of Alcohol and other Central Nervous System Depressants. Instruct patients to avoid concurrent use of Azelastine ...
more infohttps://www.drugs.com/pro/azelastine.html

Astelin - FDA prescribing information, side effects and usesAstelin - FDA prescribing information, side effects and uses

Central Nervous System Depressants. Concurrent use of Astelin Nasal Spray with alcohol or other central nervous system ... central nervous system depressants because additional reductions in alertness and additional impairment of central nervous ... Concurrent Use of Alcohol and other Central Nervous System Depressants. Instruct patients to avoid concurrent use of Astelin ... Concurrent use of Astelin Nasal Spray with alcohol or other central nervous system depressants should be avoided because ...
more infohttps://www.drugs.com/pro/astelin.html

Astepro (Azelastine Hydrochloride Nasal Spray): Side Effects, Interactions, Warning, Dosage & UsesAstepro (Azelastine Hydrochloride Nasal Spray): Side Effects, Interactions, Warning, Dosage & Uses

Central Nervous System Depressants. Concurrent use of ASTEPRO Nasal Spray with alcohol or other central nervous system ... other Central Nervous System Depressants. Avoid concurrent use of ASTEPRO with alcohol or other central nervous system ... Concurrent use of ASTEPRO with alcohol or other central nervous system depressants should be avoided because additional ... depressants should be avoided because reductions in alertness and impairment of central nervous system performance may occur [ ...
more infohttps://www.rxlist.com/astepro-drug.htm

Astelin (Azelastine Hydrochloride): Side Effects, Interactions, Warning, Dosage & UsesAstelin (Azelastine Hydrochloride): Side Effects, Interactions, Warning, Dosage & Uses

Central Nervous System Depressants. Concurrent use of Astelin Nasal Spray with alcohol or other central nervous system ... central nervous system depressants because additional reductions in alertness and additional impairment of central nervous ... Concurrent Use of Alcohol and other Central Nervous System Depressants. Instruct patients to avoid concurrent use of Astelin ... Concurrent use of Astelin Nasal Spray with alcohol or other central nervous system depressants should be avoided because ...
more infohttps://www.rxlist.com/astelin-drug.htm

Preludin
        -
        Appetite Depressants,  Central Nervous System Agents,  SympathomimeticsPreludin - Appetite Depressants, Central Nervous System Agents, Sympathomimetics

Symptoms of overdose include acute central nervous system stimulation, cardiotoxicity causing tachycardia, arrhythmias, ... Phenmetrazine is a sympathomimetic drug used primarily as an appetite depressant. Its actions and mechanisms are similar to ...
more infohttps://pharmacycode.com/Preludin.html

9 of the Most Addictive Prescription Drugs on the Market9 of the Most Addictive Prescription Drugs on the Market

Central nervous system (CNS) depressants. CNS depressants include barbiturates and benzodiazepines. Theyre also called ... It changes how your central nervous system (CNS) responds to pain. Like heroin, it creates a euphoric, sedative effect. ... Withdrawal from CNS depressants. If youre addicted to CNS depressants, youll likely develop withdrawal symptoms when you stop ... Most addictive drugs affect your brains reward system by flooding it with dopamine. This results in a pleasurable "high" that ...
more infohttps://www.healthline.com/health/addiction/addictive-prescription-drugs

Prescription Drugs - OPEN | OPEN | Northeastern UniversityPrescription Drugs - OPEN | OPEN | Northeastern University

Central Nervous System (CNS) Depressants. Sometimes referred to as sedatives and tranquilizers, used in the treatment of ... Method of action: CNS depressants work by slowing the brains activity. They can produce a drowsy or calming effect. ... Combining CNS depressants with alcohol can affect heart rhythm, slow respiration, and even lead to death. ...
more infohttp://www.northeastern.edu/open/prescription-counter-otc-medications/

Phenmetraline hydrochloride
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        Appetite Depressants,  Central Nervous System Agents,  SympathomimeticsPhenmetraline hydrochloride - Appetite Depressants, Central Nervous System Agents, Sympathomimetics

Symptoms of overdose include acute central nervous system stimulation, cardiotoxicity causing tachycardia, arrhythmias, ... Phenmetrazine is a sympathomimetic drug used primarily as an appetite depressant. Its actions and mechanisms are similar to ...
more infohttp://pharmacycode.com/Phenmetraline_hydrochloride.html

Central Nervous System Depressants - A Primer from Dayton DUICentral Nervous System Depressants - A Primer from Dayton DUI

... Lawyer Charles M. Rowland II, Call (937) 318-1384. All I do is ... CENTRAL NERVOUS SYSTEM DEPRESSANTS - A PRIMER. The category of Central Nervous System Depressants includes some of the most ... Central Nervous System Depressants. Dayton DUI Attorney Charles Rowland , DUI Law , Drugs & Alcohol , Central Nervous System ... Central nervous system agents are drugs that affect the central nervous system i.e. the brain and the spinal cord, and produce ...
more infohttps://daytondui.com/central-nervous-system-depressants-2/

Opioids facts, information, pictures | Encyclopedia.com articles about OpioidsOpioids facts, information, pictures | Encyclopedia.com articles about Opioids

Central nervous system depressant. -Any drug that tends to reduce the activity of the central nervous system. The major drug ... central nervous system depressants. *monoamine oxidase (MAO) inhibitors (a class of anti-depressants) such as furazolidone, ... Central nervous system (CNS) depressants, such as antihistamines and other medicines for allergies, hay fever, or colds; ... Alcohol and other central nervous system depressants should not be taken or consumed while opioids are being taken. ...
more infohttps://www.encyclopedia.com/medicine/drugs/pharmacology/opioids

A Guide to Central Nervous System Depressants-My Addiction InfoA Guide to Central Nervous System Depressants-My Addiction Info

Read our latest post on central nervous system depressants to get information about CNS depressants and how they work and signs ... An Overview of Central Nervous System Depressants*How Do Central Nervous System Depressants Work?*What Are the Effects of ... How Do Central Nervous System Depressants Work?. Prescriptions for CNS depressants like Xanax and Amytal and others are written ... Central Nervous System Depressant Abuse. *Millions of Americans use CNS depressants due to the euphoric high they create ...
more infohttps://myaddictioninfo.com/central-nervous-system-depressants/

Benzodiazepines: A Model for Central Nervous System (CNS) Depressants - PDFBenzodiazepines: A Model for Central Nervous System (CNS) Depressants - PDF

Depressants Objectives Summarize the basic mechanism by which benzodiazepines work in the brain. Describe two strategies for ... Central nervous system depressants (CNS depressants) Background: Benzodiazepines are a large group of drugs that act as central ... 1 Benzodiazepines: A Model for Central Nervous System (CNS) Depressants. 2 Objectives Summarize the basic mechanism by which ... 7 Pharmacodynamics: How BZDS work (cont.) Influx of Cl- causes central nervous system (CNS) depressant effect (inhibitory) ...
more infohttp://docplayer.net/4283625-Benzodiazepines-a-model-for-central-nervous-system-cns-depressants.html

DailyMed - THIORIDAZINE HYDROCHLORIDE- thioridazine hydrochloride tablet, film coatedDailyMed - THIORIDAZINE HYDROCHLORIDE- thioridazine hydrochloride tablet, film coated

Central Nervous System Depressants. As in the case of other phenothiazines, thioridazine is capable of potentiating central ... in severe central nervous system depression or comatose states from any cause including drug induced central nervous system ... Attention should be paid to the fact that phenothiazines are capable of potentiating central nervous system depressants (e.g., ... Central Nervous System. Drowsiness may be encountered on occasion, especially where large doses are given early in treatment. ...
more infohttps://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=56b3f4c2-52af-4947-b225-6808ae9f26f5

Showing Health Effect central nervous system depressant - FooDBShowing Health Effect central nervous system depressant - FooDB

central nervous system drug. ChEBI Definition. A class of drugs producing both physiological and psychological effects through ... Showing Health Effect central nervous system depressant. Identification. Name. central nervous system depressant. ...
more infohttp://foodb.ca/health_effects/812
  • Fatal respiratory depression could occur in patients who are not opioid-tolerant and in patients that are opioid-tolerant even if fentanyl transdermal system is not misused or abused. (nih.gov)
  • Fentanyl transdermal system contains fentanyl, a full opioid agonist. (nih.gov)
  • Differential modulation of gamma-aminobutyric acid receptors by caprolactam derivatives with central nervous system depressant or convulsant activity. (muscimol.xyz)
  • Sleeping pills bind to GABA receptors, which are the most common class of receptors found on the surface of nerve cells in the central nervous system (CNS). (livestrong.com)
  • NMDA receptors (NMDARs) are Ca -permeant, ligand-gated ion channels activated by the excitatory neurotransmitter glutamate and have well-characterized roles in the nervous system. (bireme.br)
  • Ethanol extract of A. aspera (EEAA) has been reported to have central antinociceptive activity in thermal-induced pain methods. (ijabmr.org)
  • It is possible to overcome an addiction to Central Nervous System depressants , but because of the dangers that come with stopping their use, it should be done under medical supervision. (4rehabilitation.com)
  • While addiction to CNS depressants is a challenge, it can be overcome. (4rehabilitation.com)
  • If you or a loved one struggles with addiction to a CNS depressant, we can help. (4rehabilitation.com)
  • Los análisis incluidos en estudios previos, que agrupan sustancias con efectos opuestos sobre el sistema nervioso central (SNC), pueden haber enmascarado la influencia de estas sobre la gravedad. (scielosp.org)
  • The signs and symptoms of CNS depressant abuse vary depending on some factors like the type of depressant abused, the size of the individual, the dosage taken, the time period of abuse, medical history, etc. (myaddictioninfo.com)
  • These highlights do not include all the information needed to use fentanyl transdermal system safely and effectively. (nih.gov)