GABA Agonists
Muscimol
GABA Antagonists
Baclofen
Receptors, GABA-A
Bicuculline
Isoxazoles
Picrotoxin
GABA Agents
Microinjections
GABA Modulators
Rats, Sprague-Dawley
Neurons
GABA Plasma Membrane Transport Proteins
Receptors, GABA-B
GABA Uptake Inhibitors
GABA-A Receptor Antagonists
Dose-Response Relationship, Drug
Nipecotic Acids
Muscarinic Agonists
Nicotinic Agonists
Adrenergic alpha-2 Receptor Agonists
Serotonin 5-HT2 Receptor Agonists
Phosphinic Acids
Neural Inhibition
Serotonin 5-HT1 Receptor Agonists
Patch-Clamp Techniques
GABA-B Receptor Antagonists
Histamine Agonists
4-Aminobutyrate Transaminase
Synaptic Transmission
Rats, Wistar
Inhibitory Postsynaptic Potentials
Pyridazines
Glutamate Decarboxylase
Diazepam
Adrenergic alpha-1 Receptor Agonists
Receptors, Opioid, mu
Cells, Cultured
Glutamic Acid
Radioligand Assay
Hippocampus
Neurite outgrowth-regulating properties of GABA and the effect of serum on mouse spinal cord neurons in culture. (1/1111)
Time-lapse photography was used to examine the effects of gamma-aminobutyric acid (GABA) on the outgrowth and motility of neurites in cultures from mouse spinal cord. GABA at concentrations of 100, 10 and 1 microM caused significant inhibition of neurite outgrowth and the motility of growth cones was significantly reduced by treatment with 100 and 10 microM GABA. This effect was mimicked by the GABA(B) receptor agonist baclofen, whereas the GABA(A) receptor agonist muscimol had no effect. The effect of GABA on outgrowth and motility seems to be dependent on the type of serum employed. The results reported here were obtained only when heat-inactivated serum was used and not when non heat-inactivated serum was added to the culture medium. They suggest that GABA has a role in the regulation of process outgrowth within the embryonic mouse spinal cord. (+info)Corticofugal amplification of facilitative auditory responses of subcortical combination-sensitive neurons in the mustached bat. (2/1111)
Recent studies on the bat's auditory system indicate that the corticofugal system mediates a highly focused positive feedback to physiologically "matched" subcortical neurons, and widespread lateral inhibition to physiologically "unmatched" subcortical neurons, to adjust and improve information processing. These findings have solved the controversy in physiological data, accumulated since 1962, of corticofugal effects on subcortical auditory neurons: inhibitory, excitatory, or both (an inhibitory effect is much more frequent than an excitatory effect). In the mustached bat, Pteronotus parnellii parnellii, the inferior colliculus, medial geniculate body, and auditory cortex each have "FM-FM" neurons, which are "combination-sensitive" and are tuned to specific time delays (echo delays) of echo FM components from the FM components of an emitted biosonar pulse. FM-FM neurons are more complex in response properties than cortical neurons which primarily respond to single tones. In the present study, we found that inactivation of the entire FM-FM area in the cortex, including neurons both physiologically matched and unmatched with subcortical FM-FM neurons, on the average reduced the facilitative responses to paired FM sounds by 82% for thalamic FM-FM neurons and by 66% for collicular FM-FM neurons. The corticofugal influence on the facilitative responses of subcortical combination-sensitive neurons is much larger than that on the excitatory responses of subcortical neurons primarily responding to single tones. Therefore we propose the hypothesis that, in general, the processing of complex sounds by combination-sensitive neurons more heavily depends on the corticofugal system than that by single-tone sensitive neurons. (+info)A single hydrophobic residue confers barbiturate sensitivity to gamma-aminobutyric acid type C receptor. (3/1111)
Barbiturate sensitivity was imparted to the human rho1 homooligomeric gamma-aminobutyric acid (GABA) receptor channel by mutation of a tryptophan residue at position 328 (Trp328), which is located within the third transmembrane domain. Substitutions of Trp328 with a spectrum of amino acids revealed that nearly all hydrophobic residues produced receptor channels that were both directly activated and modulated by pentobarbital with similar sensitivities. Previous studies with ligand-gated ion channels (including GABA) have demonstrated that even conservative amino acid substitution within the agonist-dependent activation domain (N-terminal extracellular domain) can markedly impair agonist sensitivity. Thus, the lack of significant variation in pentobarbital sensitivity among the Trp328 mutants attests to an intrinsic difference between pentobarbital- and the GABA-dependent activation domain. Compared with the heterooligomeric alphabetagamma receptor channel, the mode of modulation for homooligomeric Trp328 mutants by pentobarbital was more dependent on the GABA concentration, yielding potentiation only at low concentrations of GABA (fractions of their respective EC50 values), yet causing inhibition at higher concentrations. Agonist-related studies have also demonstrated that residue 328 plays an important role in agonist-dependent activation, suggesting a functional interconnection between the GABA and pentobarbital activation domains. (+info)Selective pruning of more active afferents when cat visual cortex is pharmacologically inhibited. (4/1111)
Activity-dependent competition is thought to guide the normal development of specific patterns of neural connections. Such competition generally favors more active inputs, making them larger and stronger, while less active inputs become smaller and weaker. We pharmacologically inhibited the activity of visual cortical cells and measured the three-dimensional structure of inputs serving the two eyes when one eye was occluded. The more active inputs serving the open eye actually became smaller than the deprived inputs from the occluded eye, which were similar to those in normal animals. These findings demonstrate in vivo that it is not the amount of afferent activity but the correlation between cortical and afferent activity that regulates the growth or retraction of these inputs. (+info)Carbamazepine facilitates effects of GABA on rat hippocampus slices. (5/1111)
AIM: To study the influence of carbamazepine (Car) on GABA effect in hippocampus. METHODS: Evoked potentials were recorded on pyramidal cells in CA1 after stimulation (0.5 Hz, 50 microseconds) to Schaffer collaterals in rat hippocampal slices (350 microns). RESULTS: Car 0.1 and 0.2 mmol.L-1 did not affect field potentials, whereas Car 0.2 mmol.L-1 plus GABA (0.1-1 mmol.L-1) gave rise to a stronger inhibition on field potentials than that of GABA alone. Bicuculline did not reverse Car facilitation on GABA inhibition on field potentials. (-)-Baclofen was more effective in inhibiting field potentials than GABA. Car 0.2 mmol.L-1 plus (-)-baclofen (1-5 mumol.L-1) brought an inhibition stronger than that of (-)-baclofen alone. CONCLUSION: Car facilitates the effects of GABA on pyramidal cells in hippocampal CA1 region, probably related to GABAB receptors. (+info)The role of gamma-hydroxybutyric acid in the treatment of alcoholism: from animal to clinical studies. (6/1111)
Since its discovery nearly 40 years ago, gamma-hydroxybutyric acid (GHB) has attracted several waves of scientific interest due to new developments in the knowledge of its mechanisms of action and ideas for its potential use in clinical practice. Its effects have been claimed to treat different psychiatric conditions, but over time its use has become limited to a few specific situations (e.g. sedating patients in non-painful surgical procedures and narcolepsy). New interest in the drug derives from its potential use in the treatment of alcoholism. Recent studies demonstrated a marked effect of the substance in suppressing ethanol (ETOH) withdrawal symptoms and in reducing craving for alcohol, compared to other available drugs. However, GHB has to be given under very careful supervision because of its side-effects, including the risk of abuse and dependence and possible interference with the metabolic pathways of endogenous GHB and ETOH. This short review discusses these and related issues and we hope that it will stimulate further interest in GHB. (+info)Tonic activation of presynaptic GABAB receptors in the opener neuromuscular junction of crayfish. (7/1111)
Release of excitatory transmitter from boutons on crayfish nerve terminals was inhibited by (R,S)-baclofen, an agonist at GABAB receptors. Baclofen had no postsynaptic actions as it reduced quantal content without affecting quantal amplitude. The effect of baclofen increased with concentration producing 18% inhibition at 10 microM; EC50, 50% inhibition at 30 microM; maximal inhibition, 85% at 100 microM and higher. There was no desensitization, even with 200 or 320 microM baclofen. Phaclofen, an antagonist at GABAB receptors, competitively antagonized the inhibitory action of baclofen (KD = 50 microM, equivalent to a pA2 = 4.3 +/- 0.1). Phaclofen on its own at concentrations below 200 microM had no effect on release, whereas at 200 microM phaclofen itself increased the control level of release by 60%, as did 2-hydroxy-saclofen (200 microM), another antagonist at GABAB receptors. This increase was evidently due to antagonism of a persistent level of GABA in the synaptic cleft, since the effect was abolished by destruction of the presynaptic inhibitory fiber, using intra-axonal pronase. We conclude that presynaptic GABAB receptors, with a pharmacological profile similar to that of mammalian GABAB receptors, are involved in the control of transmitter release at the crayfish neuromuscular junction. (+info)Inhibitory nature of tiagabine-augmented GABAA receptor-mediated depolarizing responses in hippocampal pyramidal cells. (8/1111)
Tiagabine is a potent GABA uptake inhibitor with demonstrated anticonvulsant activity. GABA uptake inhibitors are believed to produce their anticonvulsant effects by prolonging the postsynaptic actions of GABA, released during episodes of neuronal hyperexcitability. However, tiagabine has recently been reported to facilitate the depolarizing actions of GABA in the CNS of adult rats following the stimulation of inhibitory pathways at a frequency (100 Hz) intended to mimic interneuronal activation during epileptiform activity. In the present study, we performed extracellular and whole cell recordings from CA1 pyramidal neurons in rat hippocampal slices to examine the functional consequences of tiagabine-augmented GABA-mediated depolarizing responses. Orthodromic population spikes (PSs), elicited from the stratum radiatum, were inhibited following the activation of recurrent inhibitory pathways by antidromic conditioning stimulation of the alveus, which consisted of either a single stimulus or a train of stimuli delivered at high-frequency (100 Hz, 200 ms). The inhibition of orthodromic PSs produced by high-frequency conditioning stimulation (HFS), which was always of much greater strength and duration than that produced by a single conditioning stimulus, was greatly enhanced following the bath application of tiagabine (2-100 microM). Thus, in the presence of tiagabine (20 microM), orthodromic PSs, evoked 200 and 800 ms following HFS, were inhibited to 7.8 +/- 2.6% (mean +/- SE) and 34.4 +/- 18.5% of their unconditioned amplitudes compared with only 35.4 +/- 12.7% and 98.8 +/- 12.4% in control. Whole cell recordings revealed that the bath application of tiagabine (20 microM) either caused the appearance or greatly enhanced the amplitude of GABA-mediated depolarizing responses (DR). Excitatory postsynaptic potentials (EPSPs) evoked from stratum radiatum at time points that coincided with the DR were inhibited to below the threshold for action-potential firing. Independently of the stimulus intensity with which they were evoked, the charge transferred to the soma by excitatory postsynaptic currents (EPSCs), elicited in the presence of tiagabine (20 microM) during the large (1,428 +/- 331 pA) inward currents that underlie the DRs, was decreased on the average by 90.8 +/- 1.7%. Such inhibition occurred despite the presence of the GABAB receptor antagonist, CGP 52 432 (10 microM), indicating that GABAB heteroreceptors, located on glutamatergic terminals, do not mediate the observed reduction in the amplitude of excitatory postsynaptic responses. The present results suggest that despite facilitating the induction of GABA-mediated depolarizations, tiagabine application may nevertheless increase the effectiveness of synaptic inhibition during the synchronous high-frequency activation of inhibitory interneurons by enhanced shunting. (+info)GABA (gamma-aminobutyric acid) agonists are substances that bind to and activate GABA receptors in the brain, mimicking the actions of GABA, which is the primary inhibitory neurotransmitter in the central nervous system. These agents can produce various effects such as sedation, anxiolysis, muscle relaxation, and anticonvulsant activity by enhancing the inhibitory tone in the brain. They are used clinically to treat conditions such as anxiety disorders, seizures, and muscle spasticity. Examples of GABA agonists include benzodiazepines, barbiturates, and certain non-benzodiazepine hypnotics.
Muscimol is defined as a cyclic psychoactive ingredient found in certain mushrooms, including Amanita muscaria and Amanita pantherina. It acts as a potent agonist at GABA-A receptors, which are involved in inhibitory neurotransmission in the central nervous system. Muscimol can cause symptoms such as altered consciousness, delirium, hallucinations, and seizures. It is used in research but has no medical applications.
GABA-A receptor agonists are substances that bind to and activate GABA-A receptors, which are ligand-gated ion channels found in the central nervous system. GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the brain, and its activation via GABA-A receptors results in hyperpolarization of neurons and reduced neuronal excitability.
GABA-A receptor agonists can be classified into two categories: GABAergic compounds and non-GABAergic compounds. GABAergic compounds, such as muscimol and isoguvacine, are structurally similar to GABA and directly activate the receptors. Non-GABAergic compounds, on the other hand, include benzodiazepines, barbiturates, and neurosteroids, which allosterically modulate the receptor's affinity for GABA, thereby enhancing its inhibitory effects.
These agents are used in various clinical settings to treat conditions such as anxiety, insomnia, seizures, and muscle spasticity. However, they can also produce adverse effects, including sedation, cognitive impairment, respiratory depression, and physical dependence, particularly when used at high doses or for prolonged periods.
GABA (gamma-aminobutyric acid) antagonists are substances that block the action of GABA, which is the primary inhibitory neurotransmitter in the central nervous system. GABA plays a crucial role in regulating neuronal excitability and reducing the transmission of nerve impulses.
GABA antagonists work by binding to the GABA receptors without activating them, thereby preventing the normal function of GABA and increasing neuronal activity. These agents can cause excitation of the nervous system, leading to various effects depending on the specific type of GABA receptor they target.
GABA antagonists are used in medical treatments for certain conditions, such as sleep disorders, depression, and cognitive enhancement. However, they can also have adverse effects, including anxiety, agitation, seizures, and even neurotoxicity at high doses. Examples of GABA antagonists include picrotoxin, bicuculline, and flumazenil.
Baclofen is a muscle relaxant and antispastic medication. It is primarily used to treat spasticity, a common symptom in individuals with spinal cord injuries, multiple sclerosis, cerebral palsy, and other neurological disorders that can cause stiff and rigid muscles.
Baclofen works by reducing the activity of overactive nerves in the spinal cord that are responsible for muscle contractions. It binds to GABA-B receptors in the brain and spinal cord, increasing the inhibitory effects of gamma-aminobutyric acid (GABA), a neurotransmitter that helps regulate communication between nerve cells. This results in decreased muscle spasticity and improved range of motion.
The medication is available as an oral tablet or an injectable solution for intrathecal administration, which involves direct delivery to the spinal cord via a surgically implanted pump. The oral formulation is generally preferred as a first-line treatment due to its non-invasive nature and lower risk of side effects compared to intrathecal administration.
Common side effects of baclofen include drowsiness, weakness, dizziness, headache, and nausea. Intrathecal baclofen may cause more severe side effects, such as seizures, respiratory depression, and allergic reactions. Abrupt discontinuation of the medication can lead to withdrawal symptoms, including hallucinations, confusion, and increased muscle spasticity.
It is essential to consult a healthcare professional for personalized medical advice regarding the use and potential side effects of baclofen.
Gamma-Aminobutyric Acid (GABA) is a major inhibitory neurotransmitter in the mammalian central nervous system. It plays a crucial role in regulating neuronal excitability and preventing excessive neuronal firing, which helps to maintain neural homeostasis and reduce the risk of seizures. GABA functions by binding to specific receptors (GABA-A, GABA-B, and GABA-C) on the postsynaptic membrane, leading to hyperpolarization of the neuronal membrane and reduced neurotransmitter release from presynaptic terminals.
In addition to its role in the central nervous system, GABA has also been identified as a neurotransmitter in the peripheral nervous system, where it is involved in regulating various physiological processes such as muscle relaxation, hormone secretion, and immune function.
GABA can be synthesized in neurons from glutamate, an excitatory neurotransmitter, through the action of the enzyme glutamic acid decarboxylase (GAD). Once synthesized, GABA is stored in synaptic vesicles and released into the synapse upon neuronal activation. After release, GABA can be taken up by surrounding glial cells or degraded by the enzyme GABA transaminase (GABA-T) into succinic semialdehyde, which is further metabolized to form succinate and enter the Krebs cycle for energy production.
Dysregulation of GABAergic neurotransmission has been implicated in various neurological and psychiatric disorders, including epilepsy, anxiety, depression, and sleep disturbances. Therefore, modulating GABAergic signaling through pharmacological interventions or other therapeutic approaches may offer potential benefits for the treatment of these conditions.
GABA-A receptors are ligand-gated ion channels in the membrane of neuronal cells. They are the primary mediators of fast inhibitory synaptic transmission in the central nervous system. When the neurotransmitter gamma-aminobutyric acid (GABA) binds to these receptors, it opens an ion channel that allows chloride ions to flow into the neuron, resulting in hyperpolarization of the membrane and decreased excitability of the neuron. This inhibitory effect helps to regulate neural activity and maintain a balance between excitation and inhibition in the nervous system. GABA-A receptors are composed of multiple subunits, and the specific combination of subunits can determine the receptor's properties, such as its sensitivity to different drugs or neurotransmitters.
Bicuculline is a pharmacological agent that acts as a competitive antagonist at GABA-A receptors, which are inhibitory neurotransmitter receptors in the central nervous system. By blocking the action of GABA (gamma-aminobutyric acid) at these receptors, bicuculline can increase neuronal excitability and cause convulsions. It is used in research to study the role of GABAergic neurotransmission in various physiological processes and neurological disorders.
GABA-B receptor agonists are substances that bind to and activate GABA-B receptors, which are G protein-coupled receptors found in the central nervous system. GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the brain, and its activation leads to decreased neuronal excitability.
GABA-B receptor agonists can produce various effects on the body, including sedation, anxiolysis, analgesia, and anticonvulsant activity. Some examples of GABA-B receptor agonists include baclofen, gabapentin, and pregabalin. These drugs are used in the treatment of a variety of medical conditions, such as muscle spasticity, epilepsy, and neuropathic pain.
It's important to note that while GABA-B receptor agonists can have therapeutic effects, they can also produce side effects such as dizziness, weakness, and respiratory depression, especially at high doses or in overdose situations. Therefore, these drugs should be used with caution and under the supervision of a healthcare provider.
Isoxazoles are not a medical term, but a chemical compound. They are organic compounds containing a five-membered ring consisting of one nitrogen atom, one oxygen atom, and three carbon atoms. Isoxazoles have various applications in the pharmaceutical industry as they can be used to synthesize different drugs. Some isoxazole derivatives have been studied for their potential medicinal properties, such as anti-inflammatory, analgesic, and antipyretic effects. However, isoxazoles themselves are not a medical diagnosis or treatment.
Picrotoxin is a toxic, white, crystalline compound that is derived from the seeds of the Asian plant Anamirta cocculus (also known as Colchicum luteum or C. autummale). It is composed of two stereoisomers, picrotin and strychnine, in a 1:2 ratio.
Medically, picrotoxin has been used as an antidote for barbiturate overdose and as a stimulant to the respiratory center in cases of respiratory depression caused by various drugs or conditions. However, its use is limited due to its narrow therapeutic index and potential for causing seizures and other adverse effects.
Picrotoxin works as a non-competitive antagonist at GABA (gamma-aminobutyric acid) receptors in the central nervous system, blocking the inhibitory effects of GABA and increasing neuronal excitability. This property also makes it a convulsant agent and explains its use as a research tool to study seizure mechanisms and as an insecticide.
It is important to note that picrotoxin should only be used under medical supervision, and its handling requires appropriate precautions due to its high toxicity.
GABA (gamma-aminobutyric acid) agents are pharmaceutical drugs that act as agonists at the GABA receptors in the brain. GABA is the primary inhibitory neurotransmitter in the central nervous system, and it plays a crucial role in regulating neuronal excitability.
GABA agents can enhance the activity of GABA by increasing the frequency or duration of GABA-mediated chloride currents at the GABA receptors. These drugs are often used as anticonvulsants, anxiolytics, muscle relaxants, and sedatives due to their ability to reduce neuronal excitability and promote relaxation.
Examples of GABA agents include benzodiazepines, barbiturates, non-benzodiazepine hypnotics, and certain anticonvulsant drugs such as gabapentin and pregabalin. It is important to note that while these drugs can be effective in treating various medical conditions, they also carry the risk of dependence, tolerance, and adverse effects, particularly when used at high doses or for prolonged periods.
Microinjection is a medical technique that involves the use of a fine, precise needle to inject small amounts of liquid or chemicals into microscopic structures, cells, or tissues. This procedure is often used in research settings to introduce specific substances into individual cells for study purposes, such as introducing DNA or RNA into cell nuclei to manipulate gene expression.
In clinical settings, microinjections may be used in various medical and cosmetic procedures, including:
1. Intracytoplasmic Sperm Injection (ICSI): A type of assisted reproductive technology where a single sperm is injected directly into an egg to increase the chances of fertilization during in vitro fertilization (IVF) treatments.
2. Botulinum Toxin Injections: Microinjections of botulinum toxin (Botox, Dysport, or Xeomin) are used for cosmetic purposes to reduce wrinkles and fine lines by temporarily paralyzing the muscles responsible for their formation. They can also be used medically to treat various neuromuscular disorders, such as migraines, muscle spasticity, and excessive sweating (hyperhidrosis).
3. Drug Delivery: Microinjections may be used to deliver drugs directly into specific tissues or organs, bypassing the systemic circulation and potentially reducing side effects. This technique can be particularly useful in treating localized pain, delivering growth factors for tissue regeneration, or administering chemotherapy agents directly into tumors.
4. Gene Therapy: Microinjections of genetic material (DNA or RNA) can be used to introduce therapeutic genes into cells to treat various genetic disorders or diseases, such as cystic fibrosis, hemophilia, or cancer.
Overall, microinjection is a highly specialized and precise technique that allows for the targeted delivery of substances into small structures, cells, or tissues, with potential applications in research, medical diagnostics, and therapeutic interventions.
GABA (gamma-aminobutyric acid) modulators are substances that affect the function of GABA, which is the primary inhibitory neurotransmitter in the central nervous system. GABA plays a crucial role in regulating neuronal excitability and reducing the activity of overactive nerve cells.
GABA modulators can either enhance or decrease the activity of GABA receptors, depending on their specific mechanism of action. These substances can be classified into two main categories:
1. Positive allosteric modulators (PAMs): These compounds bind to a site on the GABA receptor that is distinct from the neurotransmitter binding site and enhance the activity of GABA at the receptor, leading to increased inhibitory signaling in the brain. Examples of positive allosteric modulators include benzodiazepines, barbiturates, and certain non-benzodiazepine drugs used for anxiolysis, sedation, and muscle relaxation.
2. Negative allosteric modulators (NAMs): These compounds bind to a site on the GABA receptor that reduces the activity of GABA at the receptor, leading to decreased inhibitory signaling in the brain. Examples of negative allosteric modulators include certain antiepileptic drugs and alcohol, which can reduce the effectiveness of GABA-mediated inhibition and contribute to their proconvulsant effects.
It is important to note that while GABA modulators can have therapeutic benefits in treating various neurological and psychiatric conditions, they can also carry risks for abuse, dependence, and adverse side effects, particularly when used at high doses or over extended periods.
Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.
Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.
These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.
Neurons, also known as nerve cells or neurocytes, are specialized cells that constitute the basic unit of the nervous system. They are responsible for receiving, processing, and transmitting information and signals within the body. Neurons have three main parts: the dendrites, the cell body (soma), and the axon. The dendrites receive signals from other neurons or sensory receptors, while the axon transmits these signals to other neurons, muscles, or glands. The junction between two neurons is called a synapse, where neurotransmitters are released to transmit the signal across the gap (synaptic cleft) to the next neuron. Neurons vary in size, shape, and structure depending on their function and location within the nervous system.
GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the mammalian central nervous system. GABA plasma membrane transport proteins, also known as GATs (GABA transporters), are a family of membrane-spanning proteins responsible for the uptake of GABA from the extracellular space into neurons and glial cells.
There are four main subtypes of GATs in mammals, named GAT1, GAT2, GAT3, and Betaine/GABA transporter 1 (BGT1). These transport proteins play a crucial role in terminating the synaptic transmission of GABA and regulating its concentration in the extracellular space. They also help maintain the balance between excitation and inhibition in the central nervous system.
GATs are targets for various pharmacological interventions, as modulation of their activity can affect GABAergic neurotransmission and have therapeutic potential in treating several neurological disorders, such as epilepsy, anxiety, and chronic pain.
Dopamine agonists are a class of medications that mimic the action of dopamine, a neurotransmitter in the brain that regulates movement, emotion, motivation, and reinforcement of rewarding behaviors. These medications bind to dopamine receptors in the brain and activate them, leading to an increase in dopaminergic activity.
Dopamine agonists are used primarily to treat Parkinson's disease, a neurological disorder characterized by motor symptoms such as tremors, rigidity, bradykinesia (slowness of movement), and postural instability. By increasing dopaminergic activity in the brain, dopamine agonists can help alleviate some of these symptoms.
Examples of dopamine agonists include:
1. Pramipexole (Mirapex)
2. Ropinirole (Requip)
3. Rotigotine (Neupro)
4. Apomorphine (Apokyn)
Dopamine agonists may also be used off-label to treat other conditions, such as restless legs syndrome or certain types of dopamine-responsive dystonia. However, these medications can have significant side effects, including nausea, dizziness, orthostatic hypotension, compulsive behaviors (such as gambling, shopping, or sexual addiction), and hallucinations. Therefore, they should be used with caution and under the close supervision of a healthcare provider.
GABA-B receptors are a type of G protein-coupled receptor that is activated by the neurotransmitter gamma-aminobutyric acid (GABA). These receptors are found throughout the central nervous system and play a role in regulating neuronal excitability. When GABA binds to GABA-B receptors, it causes a decrease in the release of excitatory neurotransmitters and an increase in the release of inhibitory neurotransmitters, which results in a overall inhibitory effect on neuronal activity. GABA-B receptors are involved in a variety of physiological processes, including the regulation of muscle tone, cardiovascular function, and pain perception. They have also been implicated in the pathophysiology of several neurological and psychiatric disorders, such as epilepsy, anxiety, and addiction.
GABA (gamma-aminobutyric acid) uptake inhibitors are a class of drugs or compounds that block the reuptake of GABA, an inhibitory neurotransmitter in the brain, into the presynaptic neuron. By blocking the reuptake, GABA uptake inhibitors increase the concentration of GABA in the synaptic cleft, which can enhance its inhibitory effects on neural activity. These drugs are sometimes used in the treatment of various neurological and psychiatric conditions, such as anxiety disorders, epilepsy, and spasticity. Examples of GABA uptake inhibitors include tiagabine and vigabatrin.
GABA-A receptor antagonists are pharmacological agents that block the action of gamma-aminobutyric acid (GABA) at GABA-A receptors. GABA is the primary inhibitory neurotransmitter in the central nervous system, and it exerts its effects by binding to GABA-A receptors, which are ligand-gated chloride channels. When GABA binds to these receptors, it opens the chloride channel, leading to an influx of chloride ions into the neuron and hyperpolarization of the membrane, making it less likely to fire.
GABA-A receptor antagonists work by binding to the GABA-A receptor and preventing GABA from binding, thereby blocking the inhibitory effects of GABA. This can lead to increased neuronal excitability and can result in a variety of effects depending on the specific antagonist and the location of the receptors involved.
GABA-A receptor antagonists have been used in research to study the role of GABA in various physiological processes, and some have been investigated as potential therapeutic agents for conditions such as anxiety, depression, and insomnia. However, their use is limited by their potential to cause seizures and other adverse effects due to excessive neuronal excitation. Examples of GABA-A receptor antagonists include picrotoxin, bicuculline, and flumazenil.
A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.
The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.
The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.
In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.
Purinergic P1 receptor agonists are substances that bind to and activate purinergic P1 receptors, which are a type of G protein-coupled receptor found in many tissues throughout the body. These receptors are activated by endogenous nucleotides such as adenosine and its metabolites.
Purinergic P1 receptors include four subtypes: A1, A2A, A2B, and A3. Each of these subtypes has distinct signaling pathways and physiological roles. For example, A1 receptor activation can lead to vasodilation, bradycardia, and anti-inflammatory effects, while A2A receptor activation can increase cyclic AMP levels and have anti-inflammatory effects.
Purinergic P1 receptor agonists are used in various therapeutic applications, including as cardiovascular drugs, antiplatelet agents, and anti-inflammatory agents. Some examples of purinergic P1 receptor agonists include adenosine, regadenoson, and dipyridamole.
It's important to note that the use of these substances should be under medical supervision due to their potential side effects and interactions with other medications.
Nipecotic acids are a class of compounds that function as GABA transaminase inhibitors. GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the central nervous system, and its levels are regulated by enzymes such as GABA transaminase.
Nipecotic acids work by inhibiting this enzyme, leading to an increase in GABA levels in the brain. This can have various effects on the nervous system, including sedative, hypnotic, and anticonvulsant actions. Some nipecotic acid derivatives are used in research as tools for studying the role of GABA in the brain, while others have been investigated for their potential therapeutic uses in treating conditions such as anxiety, insomnia, and epilepsy.
It's important to note that nipecotic acids and their derivatives can have significant side effects and toxicity, and they are not approved for use as medications in most countries. Therefore, they should only be used under the close supervision of a trained medical professional for research purposes.
Muscarinic agonists are a type of medication that binds to and activates muscarinic acetylcholine receptors, which are found in various organ systems throughout the body. These receptors are activated naturally by the neurotransmitter acetylcholine, and when muscarinic agonists bind to them, they mimic the effects of acetylcholine.
Muscarinic agonists can have a range of effects on different organ systems, depending on which receptors they activate. For example, they may cause bronchodilation (opening up of the airways) in the respiratory system, decreased heart rate and blood pressure in the cardiovascular system, increased glandular secretions in the gastrointestinal and salivary systems, and relaxation of smooth muscle in the urinary and reproductive systems.
Some examples of muscarinic agonists include pilocarpine, which is used to treat dry mouth and glaucoma, and bethanechol, which is used to treat urinary retention. It's important to note that muscarinic agonists can also have side effects, such as sweating, nausea, vomiting, and diarrhea, due to their activation of receptors in various organ systems.
Nicotinic agonists are substances that bind to and activate nicotinic acetylcholine receptors (nAChRs), which are ligand-gated ion channels found in the nervous system of many organisms, including humans. These receptors are activated by the endogenous neurotransmitter acetylcholine and the exogenous compound nicotine.
When a nicotinic agonist binds to the receptor, it triggers a conformational change that leads to the opening of an ion channel, allowing the influx of cations such as calcium, sodium, and potassium. This ion flux can depolarize the postsynaptic membrane and generate or modulate electrical signals in excitable tissues, such as neurons and muscles.
Nicotinic agonists have various therapeutic and recreational uses, but they can also produce harmful effects, depending on the dose, duration of exposure, and individual sensitivity. Some examples of nicotinic agonists include:
1. Nicotine: A highly addictive alkaloid found in tobacco plants, which is the prototypical nicotinic agonist. It is used in smoking cessation therapies, such as nicotine gum and patches, but it can also lead to dependence and various health issues when consumed through smoking or vaping.
2. Varenicline: A medication approved for smoking cessation that acts as a partial agonist of nAChRs. It reduces the rewarding effects of nicotine and alleviates withdrawal symptoms, helping smokers quit.
3. Rivastigmine: A cholinesterase inhibitor used to treat Alzheimer's disease and other forms of dementia. It increases the concentration of acetylcholine in the synaptic cleft, enhancing its activity at nicotinic receptors and improving cognitive function.
4. Succinylcholine: A neuromuscular blocking agent used during surgical procedures to induce paralysis and facilitate intubation. It acts as a depolarizing nicotinic agonist, causing transient muscle fasciculations followed by prolonged relaxation.
5. Curare and related compounds: Plant-derived alkaloids that act as competitive antagonists of nicotinic receptors. They are used in anesthesia to induce paralysis and facilitate mechanical ventilation during surgery.
In summary, nicotinic agonists are substances that bind to and activate nicotinic acetylcholine receptors, leading to various physiological responses. These compounds have diverse applications in medicine, from smoking cessation therapies to treatments for neurodegenerative disorders and anesthesia. However, they can also pose risks when misused or abused, as seen with nicotine addiction and the potential side effects of certain medications.
Adrenergic alpha-2 receptor agonists are a class of medications that bind to and activate adrenergic alpha-2 receptors, which are found in the nervous system and other tissues. These receptors play a role in regulating various bodily functions, including blood pressure, heart rate, and release of certain hormones.
When adrenergic alpha-2 receptor agonists bind to these receptors, they can cause a variety of effects, such as:
* Vasoconstriction (narrowing of blood vessels), which can increase blood pressure
* Decreased heart rate and force of heart contractions
* Suppression of the release of norepinephrine (a hormone and neurotransmitter involved in the "fight or flight" response) from nerve endings
* Analgesia (pain relief)
Adrenergic alpha-2 receptor agonists are used in a variety of medical conditions, including:
* High blood pressure
* Glaucoma (to reduce pressure in the eye)
* Anesthesia (to help prevent excessive bleeding and to provide sedation)
* Opioid withdrawal symptoms (to help manage symptoms such as anxiety, agitation, and muscle aches)
Examples of adrenergic alpha-2 receptor agonists include clonidine, brimonidine, and dexmedetomidine.
Adrenergic agonists are medications or substances that bind to and activate adrenergic receptors, which are a type of receptor in the body that respond to neurotransmitters such as norepinephrine and epinephrine (also known as adrenaline).
There are two main types of adrenergic receptors: alpha and beta receptors. Alpha-adrenergic agonists activate alpha receptors, while beta-adrenergic agonists activate beta receptors. These medications can have a variety of effects on the body, depending on which type of receptor they act on.
Alpha-adrenergic agonists are often used to treat conditions such as nasal congestion, glaucoma, and low blood pressure. Examples include phenylephrine, oxymetazoline, and clonidine.
Beta-adrenergic agonists are commonly used to treat respiratory conditions such as asthma and COPD (chronic obstructive pulmonary disease). They work by relaxing the smooth muscle in the airways, which makes it easier to breathe. Examples include albuterol, salmeterol, and formoterol.
It's important to note that adrenergic agonists can have both desired and undesired effects on the body. They should be used under the guidance of a healthcare professional, who can monitor their effectiveness and potential side effects.
Serotonin 5-HT2 receptor agonists are a class of compounds that bind to and activate the serotonin 5-HT2 receptors, which are a type of G protein-coupled receptor found in the central and peripheral nervous systems. These receptors play important roles in various physiological processes, including neurotransmission, vasoconstriction, and smooth muscle contraction.
Serotonin 5-HT2 receptor agonists can produce a range of effects depending on the specific subtype of receptor they activate. For example, activation of 5-HT2A receptors has been associated with hallucinogenic effects, while activation of 5-HT2B receptors has been linked to cardiac valvulopathy.
These drugs are used in a variety of clinical settings, including the treatment of psychiatric disorders such as depression and schizophrenia, migraine headaches, and cluster headaches. Examples of serotonin 5-HT2 receptor agonists include LSD, psilocybin, ergotamine, and sumatriptan.
I'm sorry for any confusion, but "Phosphinic Acids" is not a recognized medical term. Phosphinic acids are chemical compounds that contain a phosphorus atom bonded to two organic groups and one hydroxyl group, making them a subclass of organophosphorus compounds. They are widely used in the production of various chemicals, but they do not have specific relevance to medical definitions or terminology. If you have any questions related to medicine or health, I'd be happy to try to help answer those!
Neural inhibition is a process in the nervous system that decreases or prevents the activity of neurons (nerve cells) in order to regulate and control communication within the nervous system. It is a fundamental mechanism that allows for the balance of excitation and inhibition necessary for normal neural function. Inhibitory neurotransmitters, such as GABA (gamma-aminobutyric acid) and glycine, are released from the presynaptic neuron and bind to receptors on the postsynaptic neuron, reducing its likelihood of firing an action potential. This results in a decrease in neural activity and can have various effects depending on the specific neurons and brain regions involved. Neural inhibition is crucial for many functions including motor control, sensory processing, attention, memory, and emotional regulation.
Serotonin 5-HT1 Receptor Agonists are a class of compounds that bind to and activate the serotonin 5-HT1 receptors, which are G protein-coupled receptors found in the central and peripheral nervous systems. These receptors play important roles in regulating various physiological functions, including neurotransmission, vasoconstriction, and hormone secretion.
Serotonin 5-HT1 Receptor Agonists are used in medical therapy to treat a variety of conditions, such as migraines, cluster headaches, depression, anxiety, and insomnia. Some examples of Serotonin 5-HT1 Receptor Agonists include sumatriptan, rizatriptan, zolmitriptan, naratriptan, and frovatriptan, which are used to treat migraines and cluster headaches by selectively activating the 5-HT1B/1D receptors in cranial blood vessels and sensory nerves.
Other Serotonin 5-HT1 Receptor Agonists, such as buspirone, are used to treat anxiety disorders and depression by acting on the 5-HT1A receptors in the brain. These drugs work by increasing serotonergic neurotransmission, which helps to regulate mood, cognition, and behavior.
Overall, Serotonin 5-HT1 Receptor Agonists are a valuable class of drugs that have shown efficacy in treating various neurological and psychiatric conditions. However, like all medications, they can have side effects and potential drug interactions, so it is important to use them under the guidance of a healthcare professional.
Patch-clamp techniques are a group of electrophysiological methods used to study ion channels and other electrical properties of cells. These techniques were developed by Erwin Neher and Bert Sakmann, who were awarded the Nobel Prize in Physiology or Medicine in 1991 for their work. The basic principle of patch-clamp techniques involves creating a high resistance seal between a glass micropipette and the cell membrane, allowing for the measurement of current flowing through individual ion channels or groups of channels.
There are several different configurations of patch-clamp techniques, including:
1. Cell-attached configuration: In this configuration, the micropipette is attached to the outer surface of the cell membrane, and the current flowing across a single ion channel can be measured. This configuration allows for the study of the properties of individual channels in their native environment.
2. Whole-cell configuration: Here, the micropipette breaks through the cell membrane, creating a low resistance electrical connection between the pipette and the inside of the cell. This configuration allows for the measurement of the total current flowing across all ion channels in the cell membrane.
3. Inside-out configuration: In this configuration, the micropipette is pulled away from the cell after establishing a seal, resulting in the exposure of the inner surface of the cell membrane to the solution in the pipette. This configuration allows for the study of the properties of ion channels in isolation from other cellular components.
4. Outside-out configuration: Here, the micropipette is pulled away from the cell after establishing a seal, resulting in the exposure of the outer surface of the cell membrane to the solution in the pipette. This configuration allows for the study of the properties of ion channels in their native environment, but with the ability to control the composition of the extracellular solution.
Patch-clamp techniques have been instrumental in advancing our understanding of ion channel function and have contributed to numerous breakthroughs in neuroscience, pharmacology, and physiology.
GABA-B receptor antagonists are pharmacological agents that block the activation of GABA-B receptors, which are G protein-coupled receptors found in the central and peripheral nervous systems. Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the brain, and it exerts its effects by binding to GABA-A and GABA-B receptors.
GABA-B receptor antagonists work by preventing GABA from binding to these receptors, thereby blocking the inhibitory effects of GABA. This can lead to increased neuronal excitability and can have various pharmacological effects depending on the specific receptor subtype and location in the body.
GABA-B receptor antagonists have been investigated for their potential therapeutic use in a variety of neurological and psychiatric disorders, such as epilepsy, depression, anxiety, and substance abuse disorders. However, their clinical use is still not well established due to limited efficacy and potential side effects, including increased anxiety, agitation, and seizures.
Histamine agonists are substances that bind to and activate histamine receptors, leading to the initiation or enhancement of various physiological responses. Histamine is a naturally occurring molecule that plays a key role in the body's immune and allergic responses, as well as in the regulation of sleep, wakefulness, and appetite.
There are four main types of histamine receptors (H1, H2, H3, and H4), each with distinct functions and signaling pathways. Histamine agonists can be selective for one or more of these receptor subtypes, depending on their pharmacological properties.
For example, H1 agonists are commonly used as decongestants and antihistamines to treat allergies, while H2 agonists are used to treat gastroesophageal reflux disease (GERD) and peptic ulcers. H3 agonists have been investigated for their potential therapeutic use in the treatment of neurological disorders such as Parkinson's disease and schizophrenia, while H4 agonists are being studied for their role in inflammation and immune regulation.
It is important to note that histamine agonists can also have adverse effects, particularly if they are not selective for a specific receptor subtype or if they are used at high doses. These effects may include increased heart rate, blood pressure, and bronchodilation (opening of the airways), as well as gastrointestinal symptoms such as nausea, vomiting, and diarrhea.
Purinergic P2 receptor agonists are substances that bind and activate purinergic P2 receptors, which are a type of cell surface receptor found in many tissues throughout the body. These receptors are activated by extracellular nucleotides, such as ATP (adenosine triphosphate) and ADP (adenosine diphosphate), and play important roles in various physiological processes, including neurotransmission, muscle contraction, and inflammation.
P2 receptors are divided into two main subfamilies: P2X and P2Y. P2X receptors are ligand-gated ion channels that allow the flow of ions across the cell membrane when activated, while P2Y receptors are G protein-coupled receptors that activate intracellular signaling pathways.
Purinergic P2 receptor agonists can be synthetic or naturally occurring compounds that selectively bind to and activate specific subtypes of P2 receptors. They have potential therapeutic applications in various medical conditions, such as pain management, cardiovascular diseases, and neurological disorders. However, their use must be carefully monitored due to the potential for adverse effects, including desensitization of receptors and activation of unwanted signaling pathways.
Excitatory amino acid agonists are substances that bind to and activate excitatory amino acid receptors, leading to an increase in the excitation or activation of neurons. The most common excitatory amino acids in the central nervous system are glutamate and aspartate.
Agonists of excitatory amino acid receptors can be divided into two main categories: ionotropic and metabotropic. Ionotropic receptors, such as N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainite receptors, are ligand-gated ion channels that directly mediate fast excitatory synaptic transmission. Metabotropic receptors, on the other hand, are G protein-coupled receptors that modulate synaptic activity through second messenger systems.
Excitatory amino acid agonists have been implicated in various physiological and pathophysiological processes, including learning and memory, neurodevelopment, and neurodegenerative disorders such as stroke, epilepsy, and Alzheimer's disease. They are also used in research to study the functions of excitatory amino acid receptors and their roles in neuronal signaling. However, due to their potential neurotoxic effects, the therapeutic use of excitatory amino acid agonists is limited.
Adrenergic beta-agonists are a class of medications that bind to and activate beta-adrenergic receptors, which are found in various tissues throughout the body. These receptors are part of the sympathetic nervous system and mediate the effects of the neurotransmitter norepinephrine (also called noradrenaline) and the hormone epinephrine (also called adrenaline).
When beta-agonists bind to these receptors, they stimulate a range of physiological responses, including relaxation of smooth muscle in the airways, increased heart rate and contractility, and increased metabolic rate. As a result, adrenergic beta-agonists are often used to treat conditions such as asthma, chronic obstructive pulmonary disease (COPD), and bronchitis, as they can help to dilate the airways and improve breathing.
There are several different types of beta-agonists, including short-acting and long-acting formulations. Short-acting beta-agonists (SABAs) are typically used for quick relief of symptoms, while long-acting beta-agonists (LABAs) are used for more sustained symptom control. Examples of adrenergic beta-agonists include albuterol (also known as salbutamol), terbutaline, formoterol, and salmeterol.
It's worth noting that while adrenergic beta-agonists can be very effective in treating respiratory conditions, they can also have side effects, particularly if used in high doses or for prolonged periods of time. These may include tremors, anxiety, palpitations, and increased blood pressure. As with any medication, it's important to use adrenergic beta-agonists only as directed by a healthcare professional.
Cholinergic agonists are substances that bind to and activate cholinergic receptors, which are neuroreceptors that respond to the neurotransmitter acetylcholine. These agents can mimic the effects of acetylcholine in the body and are used in medical treatment to produce effects such as pupil constriction, increased gastrointestinal motility, bronchodilation, and improved cognition. Examples of cholinergic agonists include pilocarpine, bethanechol, and donepezil.
4-Aminobutyrate transaminase (GABA transaminase or GABA-T) is an enzyme that catalyzes the reversible transfer of an amino group from 4-aminobutyrate (GABA) to 2-oxoglutarate, forming succinic semialdehyde and glutamate. This enzyme plays a crucial role in the metabolism of the major inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the central nervous system. Inhibition of GABA transaminase is a therapeutic strategy for the treatment of various neurological disorders, such as epilepsy and anxiety, due to its ability to increase GABA levels in the brain.
Synaptic transmission is the process by which a neuron communicates with another cell, such as another neuron or a muscle cell, across a junction called a synapse. It involves the release of neurotransmitters from the presynaptic terminal of the neuron, which then cross the synaptic cleft and bind to receptors on the postsynaptic cell, leading to changes in the electrical or chemical properties of the target cell. This process is critical for the transmission of signals within the nervous system and for controlling various physiological functions in the body.
"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.
Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.
Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.
Adenosine A1 receptor agonists are medications or substances that bind to and activate the adenosine A1 receptors, which are found on the surface of certain cells in the body, including those in the heart, brain, and other organs.
Adenosine is a naturally occurring molecule in the body that helps regulate various physiological processes, such as cardiovascular function and neurotransmission. The adenosine A1 receptor plays an important role in modulating the activity of the heart, including reducing heart rate and lowering blood pressure.
Adenosine A1 receptor agonists are used clinically to treat certain medical conditions, such as supraventricular tachycardia (a rapid heart rhythm originating from above the ventricles), and to prevent cerebral vasospasm (narrowing of blood vessels in the brain) following subarachnoid hemorrhage.
Examples of adenosine A1 receptor agonists include adenosine, regadenoson, and capadenoson. These medications work by mimicking the effects of naturally occurring adenosine on the A1 receptors, leading to a decrease in heart rate and blood pressure.
It's important to note that adenosine A1 receptor agonists can have side effects, such as chest pain, shortness of breath, and flushing, which are usually transient and mild. However, they should be used with caution and under the supervision of a healthcare professional, as they can also have more serious side effects in certain individuals.
Inhibitory postsynaptic potentials (IPSPs) are electrical signals that occur in the postsynaptic neuron when an inhibitory neurotransmitter is released from the presynaptic neuron and binds to receptors on the postsynaptic membrane. This binding causes a decrease in the excitability of the postsynaptic neuron, making it less likely to fire an action potential.
IPSPs are typically caused by neurotransmitters such as gamma-aminobutyric acid (GABA) and glycine, which open chloride channels in the postsynaptic membrane. The influx of negatively charged chloride ions into the neuron causes a hyperpolarization of the membrane potential, making it more difficult for the neuron to reach the threshold needed to generate an action potential.
IPSPs play an important role in regulating the activity of neural circuits and controlling the flow of information through the nervous system. By inhibiting the activity of certain neurons, IPSPs can help to sharpen the signals that are transmitted between neurons and prevent unwanted noise or interference from disrupting communication within the circuit.
Adrenergic alpha-agonists are a type of medication that binds to and activates adrenergic alpha receptors, which are found in the nervous system and other tissues throughout the body. These receptors are activated naturally by chemicals called catecholamines, such as norepinephrine and epinephrine (also known as adrenaline), that are released in response to stress or excitement.
When adrenergic alpha-agonists bind to these receptors, they mimic the effects of catecholamines and cause various physiological responses, such as vasoconstriction (constriction of blood vessels), increased heart rate and force of heart contractions, and relaxation of smooth muscle in the airways.
Adrenergic alpha-agonists are used to treat a variety of medical conditions, including hypertension (high blood pressure), glaucoma, nasal congestion, and attention deficit hyperactivity disorder (ADHD). Examples of adrenergic alpha-agonists include phenylephrine, clonidine, and guanfacine.
It's important to note that adrenergic alpha-agonists can have both beneficial and harmful effects, depending on the specific medication, dosage, and individual patient factors. Therefore, they should only be used under the guidance of a healthcare professional.
I apologize for any confusion, but "Pyridazines" is not a medical term. It is a chemical term that refers to a class of heterocyclic organic compounds which contain a six-membered ring with two nitrogen atoms. These types of compounds are often used in the synthesis of various pharmaceuticals and agrochemicals, but "Pyridazines" itself is not a medical concept or diagnosis. If you have any questions related to medicine or health, I would be happy to try to help answer those for you.
Glutamate decarboxylase (GAD) is an enzyme that plays a crucial role in the synthesis of the neurotransmitter gamma-aminobutyric acid (GABA) in the brain. GABA is an inhibitory neurotransmitter that helps to balance the excitatory effects of glutamate, another neurotransmitter.
Glutamate decarboxylase catalyzes the conversion of glutamate to GABA by removing a carboxyl group from the glutamate molecule. This reaction occurs in two steps, with the enzyme first converting glutamate to glutamic acid semialdehyde and then converting that intermediate product to GABA.
There are two major isoforms of glutamate decarboxylase, GAD65 and GAD67, which differ in their molecular weight, subcellular localization, and function. GAD65 is primarily responsible for the synthesis of GABA in neuronal synapses, while GAD67 is responsible for the synthesis of GABA in the cell body and dendrites of neurons.
Glutamate decarboxylase is an important target for research in neurology and psychiatry because dysregulation of GABAergic neurotransmission has been implicated in a variety of neurological and psychiatric disorders, including epilepsy, anxiety, depression, and schizophrenia.
Diazepam is a medication from the benzodiazepine class, which typically has calming, sedative, muscle relaxant, and anticonvulsant properties. Its medical uses include the treatment of anxiety disorders, alcohol withdrawal syndrome, end-of-life sedation, seizures, muscle spasms, and as a premedication for medical procedures. Diazepam is available in various forms, such as tablets, oral solution, rectal gel, and injectable solutions. It works by enhancing the effects of a neurotransmitter called gamma-aminobutyric acid (GABA) in the brain, which results in the modulation of nerve impulses in the brain, producing a sedative effect.
It is important to note that diazepam can be habit-forming and has several potential side effects, including drowsiness, dizziness, weakness, and impaired coordination. It should only be used under the supervision of a healthcare professional and according to the prescribed dosage to minimize the risk of adverse effects and dependence.
Adrenergic alpha-1 receptor agonists are a type of medication that binds to and activates adrenergic alpha-1 receptors, which are found in various tissues throughout the body, including the smooth muscle of blood vessels, the heart, the liver, and the kidneys. When these receptors are activated, they cause a variety of physiological responses, such as vasoconstriction (constriction of blood vessels), increased heart rate and force of heart contractions, and relaxation of the detrusor muscle in the bladder.
Examples of adrenergic alpha-1 receptor agonists include phenylephrine, which is used to treat low blood pressure and nasal congestion, and midodrine, which is used to treat orthostatic hypotension (low blood pressure upon standing). These medications can have side effects such as increased heart rate, headache, and anxiety. It's important to use them under the supervision of a healthcare provider, as they may interact with other medications and medical conditions.
Opioid mu receptors, also known as mu-opioid receptors (MORs), are a type of G protein-coupled receptor that binds to opioids, a class of chemicals that include both natural and synthetic painkillers. These receptors are found in the brain, spinal cord, and gastrointestinal tract, and play a key role in mediating the effects of opioid drugs such as morphine, heroin, and oxycodone.
MORs are involved in pain modulation, reward processing, respiratory depression, and physical dependence. Activation of MORs can lead to feelings of euphoria, decreased perception of pain, and slowed breathing. Prolonged activation of these receptors can also result in tolerance, where higher doses of the drug are required to achieve the same effect, and dependence, where withdrawal symptoms occur when the drug is discontinued.
MORs have three main subtypes: MOR-1, MOR-2, and MOR-3, with MOR-1 being the most widely studied and clinically relevant. Selective agonists for MOR-1, such as fentanyl and sufentanil, are commonly used in anesthesia and pain management. However, the abuse potential and risk of overdose associated with these drugs make them a significant public health concern.
"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.
Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.
It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.
Glutamic acid is an alpha-amino acid, which is one of the 20 standard amino acids in the genetic code. The systematic name for this amino acid is (2S)-2-Aminopentanedioic acid. Its chemical formula is HO2CCH(NH2)CH2CH2CO2H.
Glutamic acid is a crucial excitatory neurotransmitter in the human brain, and it plays an essential role in learning and memory. It's also involved in the metabolism of sugars and amino acids, the synthesis of proteins, and the removal of waste nitrogen from the body.
Glutamic acid can be found in various foods such as meat, fish, beans, eggs, dairy products, and vegetables. In the human body, glutamic acid can be converted into gamma-aminobutyric acid (GABA), another important neurotransmitter that has a calming effect on the nervous system.
A radioligand assay is a type of in vitro binding assay used in molecular biology and pharmacology to measure the affinity and quantity of a ligand (such as a drug or hormone) to its specific receptor. In this technique, a small amount of a radioactively labeled ligand, also known as a radioligand, is introduced to a sample containing the receptor of interest. The radioligand binds competitively with other unlabeled ligands present in the sample for the same binding site on the receptor. After allowing sufficient time for binding, the reaction is stopped, and the amount of bound radioligand is measured using a technique such as scintillation counting. The data obtained from this assay can be used to determine the dissociation constant (Kd) and maximum binding capacity (Bmax) of the receptor-ligand interaction, which are important parameters in understanding the pharmacological properties of drugs and other ligands.
The hippocampus is a complex, curved formation in the brain that resembles a seahorse (hence its name, from the Greek word "hippos" meaning horse and "kampos" meaning sea monster). It's part of the limbic system and plays crucial roles in the formation of memories, particularly long-term ones.
This region is involved in spatial navigation and cognitive maps, allowing us to recognize locations and remember how to get to them. Additionally, it's one of the first areas affected by Alzheimer's disease, which often results in memory loss as an early symptom.
Anatomically, it consists of two main parts: the Ammon's horn (or cornu ammonis) and the dentate gyrus. These structures are made up of distinct types of neurons that contribute to different aspects of learning and memory.
Cannabinoid receptor agonists are compounds that bind to and activate cannabinoid receptors, which are part of the endocannabinoid system in the human body. These receptors are involved in various physiological processes, including pain modulation, appetite regulation, memory, and mood.
There are two main types of cannabinoid receptors: CB1 receptors, which are primarily found in the brain and central nervous system, and CB2 receptors, which are mainly found in the immune system and peripheral tissues.
Cannabinoid receptor agonists can be classified based on their chemical structure and origin. Some naturally occurring cannabinoids, such as THC (tetrahydrocannabinol) and CBD (cannabidiol), are found in the Cannabis sativa plant and can activate cannabinoid receptors. Synthetic cannabinoids, on the other hand, are human-made compounds designed to mimic or enhance the effects of natural cannabinoids.
Examples of cannabinoid receptor agonists include:
1. THC (tetrahydrocannabinol): The primary psychoactive component of marijuana, THC binds to CB1 receptors and produces feelings of euphoria or "high." It also has analgesic, anti-inflammatory, and appetite-stimulating properties.
2. CBD (cannabidiol): A non-psychoactive compound found in cannabis, CBD has a more complex interaction with the endocannabinoid system. While it does not bind strongly to CB1 or CB2 receptors, it can influence their activity and modulate the effects of other cannabinoids. CBD is known for its potential therapeutic benefits, including anti-inflammatory, analgesic, anxiolytic, and neuroprotective properties.
3. Synthetic cannabinoids: These are human-made compounds designed to mimic or enhance the effects of natural cannabinoids. Examples include dronabinol (Marinol), a synthetic THC used to treat nausea and vomiting in cancer patients, and nabilone (Cesamet), another synthetic THC used to manage pain and nausea in cancer and AIDS patients.
4. CP 55,940: A potent synthetic cannabinoid agonist that binds to both CB1 and CB2 receptors with high affinity. It is used in research to study the endocannabinoid system and its functions.
5. WIN 55,212-2: Another synthetic cannabinoid agonist that binds to both CB1 and CB2 receptors. It is often used in research to investigate the therapeutic potential of cannabinoids.
It's important to note that while some cannabinoid receptor agonists have demonstrated therapeutic benefits, they can also have side effects and potential risks, particularly when used in high doses or without medical supervision. Always consult a healthcare professional before using any cannabinoid-based medication or supplement.
GABA receptor agonist
Clobazam
Bamaluzole
Additive effect
N4-Chloroacetylcytosine arabinoside
Muscimol
Emamectin
Rapid sequence induction
Diazepam
Chlordiazepoxide
Progabide
BL-1020
Isovaline
GABA receptor
SKF-97,541
CGP-35348
Darigabat
Pitrazepin
Erminio Costa
Allopregnanolone
Rostral ventromedial medulla
Nucleus accumbens
GABAA receptor positive allosteric modulator
Gamma-aminobutyric acid receptor subunit alpha-1
Ventral tegmental area
Gamma-Amino-beta-hydroxybutyric acid
Psychoactive drug
Spinosad
TB-21007
Alcohol detoxification
GABA receptor agonist - Wikipedia
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Receptors35
- A GABA receptor agonist is a drug that is an agonist for one or more of the GABA receptors, producing typically sedative effects, and may also cause other effects such as anxiolytic, anticonvulsant, and muscle relaxant effects. (wikipedia.org)
- The two receptors GABA-α and GABA-ρ are ion channels that are permeable to chloride ions which reduces neuronal excitability. (wikipedia.org)
- The GABA-β receptor belongs to the class of G-Protein coupled receptors that inhibit adenylyl cyclase, therefore leading to decreased cyclic adenosine monophosphate (cAMP). (wikipedia.org)
- GABA-α and GABA-ρ receptors produce sedative and hypnotic effects and have anti-convulsion properties. (wikipedia.org)
- GABA-β receptors also produce sedative effects. (wikipedia.org)
- These drugs act instead as positive allosteric modulators (PAMs) and while they do bind to the GABA receptors, they bind to an allosteric site on the receptor and cannot induce a response from the neuron without an actual agonist being present. (wikipedia.org)
- However, some general anaesthetics like propofol and high doses of barbiturates may not only be positive allosteric modulators of GABA-A receptors but also direct agonists of these receptors. (wikipedia.org)
- Alcohol is believed to mimic GABA's effect in the brain, binding to GABA receptors and inhibiting neuronal signaling. (wikipedia.org)
- The influence of γ-aminobutyric type-A (GABA A ) receptors agonist (muscimol hydrobromide, 0.1 µg/0.5 µl) injections into the right or left basolateral amygdala (BLA) on the behavior of high-an- xiety (HA) and low-anxiety (LA) rats subjected to the elevated plus-maze (EPM) test was investigated. (scirp.org)
- Muscimol is a potent, selective agonist for the GABAA receptors, and displays sedative-hypnotic, depressant and hallucinogenic psychoactivity. (amanitaresearch.com)
- Neurons that produce GABA as their output are called GABAergic neurons, and have chiefly inhibitory action at receptors in the adult vertebrate. (amanitaresearch.com)
- The β-cells secrete GABA along with insulin and the GABA binds to GABA receptors on the neighboring islet α-cells and inhibits them from secreting glucagon (which would counteract insulin's effects). (amanitaresearch.com)
- Immune cells express receptors for GABA and administration of GABA can suppress inflammatory immune responses and promote "regulatory" immune responses, such that GABA administration has been shown to inhibit autoimmune diseases in several animal models. (amanitaresearch.com)
- I think it's not an issue with gaba per say but an issue with limited receptors due to the benzos. (amanitaresearch.com)
- In the vertebrate CNS, fast synaptic inhibition is mediated by GABA and glycine receptors. (ox.ac.uk)
- Currents were elicited by fast agonist application to outside-out patches from HEK-293 cells expressing rat glycine or GABA receptors. (ox.ac.uk)
- Our main finding is that glycine and GABA receptors "sense" chloride concentrations because of interactions between the M2 pore-lining domain and the permeating ions. (ox.ac.uk)
- These target and activate the GABA receptors in the brain, which promote sleepiness, she says. (sleepreviewmag.com)
- Activation of these receptors enhances the effects of GABA. (medscape.com)
- its decarboxylated derivative, muscimol, is an agonist at gamma-aminobutyric acid (GABA) receptors. (medscape.com)
- By acting on GABA receptors, Theanine mimmicks the neurotransmitter, reducing stress, easing muscle tension, and lowering blood pressure. (vagarights.com)
- The selective toxicity of isoxazolines between insects, acarines, and mammals is due to the differential sensitivity of the GABA receptors in the respective species. (merckvetmanual.com)
- GABA-B receptors are present in the brain (especially the cerebral cortex, thalamic nuclei, cerebellum, and amygdala). (emcrit.org)
- GABA-B receptors are also found in the ventral and dorsal horns of the spinal cord. (emcrit.org)
- GABA-B receptors occur outside the blood-brain barrier, within the sympathetic nervous system and some visceral tissues (including the heart). (emcrit.org)
- Among targets under investigation, cholinergic receptors have received much attention with several nicotinic agonists (α7 and α4β2) actively in clinical trials for the treatment of AD, CIAS and attention deficit hyperactivity disorder (ADHD). (sri.com)
- Phenibut works by binding to the GABA receptors in a person's brain. (consumerhealthdigest.com)
- Since it is a compound that binds to GABA receptors, with higher doses, it can cause sleepiness. (consumerhealthdigest.com)
- Although there is still no specific explanation, it is suggested that this effect is due to the compound's action on GABA-A, GABA-B and dopamine receptors. (consumerhealthdigest.com)
- Interestingly, taurine has been reported to interact with neurotransmitter receptors involved in sleep regulation, including GABA-A, GABA-B, and glycine. (life-enhancement.com)
- in many instances taurine exerted its cytoprotective effects against excitotoxic and/or energy depriving insults in vitro by a mechanism involving interaction with GABA-A receptors. (life-enhancement.com)
- This is consistent with the fact that activation of GABA-A receptors counteracts the activation of NMDA receptors and generation of nitric oxide. (life-enhancement.com)
- As of the time of the publication of this paper, however, the interaction of endogenous taurine with GABA-A receptors in vivo remained uncertain. (life-enhancement.com)
- However, they also noted that, "exogenous taurine has in many instances turned out to have profound neuroprotective effects, many of which can be ascribed to interaction with GABA-A receptors. (life-enhancement.com)
- Muscimol is a potent agonist of GABA-A RECEPTORS and is used mainly as an experimental tool in animal and tissue studies. (bvsalud.org)
Receptor agonist5
- Pagoclone is a novel, non-benzodiazepine, selective GABA-A receptor agonist. (fiercebiotech.com)
- Restoril is a benzodiazepine and Ambien is a type A GABA receptor agonist . (rxlist.com)
- It acts as a GABA A receptor agonist. (artandpopularculture.com)
- Ovid Therapeutics), a delta (δ)-selective GABA A receptor agonist, for the treatment of Fragile X syndrome. (empr.com)
- Magnesium calms down the nervous system by acting as a GABA receptor agonist. (forcesofnature.ca)
Demonstrates GABA-A agonist Activity1
- Taurine: Neuroprotective amino acid that provides antioxidant protection and demonstrates GABA-A agonist activity (7-9). (bayho.com)
Neurotransmitter5
- GABA is the major inhibitory neurotransmitter in the brain, and GABA-like drugs are used to suppress spasms. (wikipedia.org)
- Muscimol is a potent GABAA agonist, activating the receptor for the brain's principal inhibitory neurotransmitter, GABA. (amanitaresearch.com)
- Gamma-Aminobutyric acid, or γ-aminobutyric acid or GABA, is the chief inhibitory neurotransmitter in the developmentally mature mammalian central nervous system. (amanitaresearch.com)
- Phenibut is a derivative of the naturally occurring inhibitory neurotransmitter GABA capable of passing the blood-brain barrier and has been used as a nootropic, relaxation aid, and a sleep promoter. (consumerhealthdigest.com)
- This action is mediated by its agonist effects upon the inhibitory GABA (the chief inhibitory neurotransmitter in the vertebrate central nervous system. (americanaquariumproducts.com)
Muscimol6
- Muscimol binds to the same site on the GABAA receptor complex as GABA itself, as opposed to other GABAergic drugs such as barbiturates and benzodiazepines which bind to separate regulatory sites. (amanitaresearch.com)
- Muscimol is a non-addictive GABA agonist. (amanitaresearch.com)
- In RCs, an asymmetric co-responsive pattern was observed between GABA- and muscimol-evoked events. (nih.gov)
- Muscimol-sensitive RCs responded well to GABA, but not all GABA-sensitive RCs responded to muscimol. (nih.gov)
- In GABA-sensitive BCs, muscimol responses were typically weak or absent. (nih.gov)
- Many of the central nervous system (CNS) effects of muscimol (eg, sedation) are ascribed to its ability to act as a GABA agonist. (medscape.com)
Baclofen3
- Although a small minority of GABA-sensitive cells hyperpolarized in response to R(+)baclofen, bicuculline-insensitive responses were not antagonized by 2-hydroxysaclofen, and were abolished in low [Cl-]o. (nih.gov)
- Baclofen is a Gaba- b agonist that is widely used as a skeletal muscle relaxant. (medindia.net)
- Baclofen acts as an agonist of the GABA-B receptor. (emcrit.org)
Antagonists1
- They are noncompetitive GABA receptor antagonists, bind to chloride channels in nerve and muscle cells, blocking signal transmission, and cause hyperexcitation, resulting in uncontrolled activity in the CNS and death of the target. (merckvetmanual.com)
Selective1
- Pagoclone is a novel member of the cyclopyrrolone class of compounds and acts as a gamma amino butyric acid (GABA) selective receptor modulator. (fiercebiotech.com)
Neuropathic Pain1
- A single intrathecal injection of GABA permanently reverses neuropathic pain after nerve injury. (ijabbr.com)
Binds1
- Positive allosteric modulators work by increasing the frequency with which the chloride channel opens when an agonist binds to its own site on the GABA receptor. (wikipedia.org)
NMDA1
- Most of the clinical effects can be explained by the interaction of ethanol with various neurotransmitters and neuroreceptors in the brain, including those interacting with gamma-aminobutyric acid (GABA), glutamate (NMDA), and opiates. (medscape.com)
Glycine3
- Chloride ions in the pore of glycine and GABA channels shape the time course and voltage dependence of agonist currents. (ox.ac.uk)
- Here we extend these findings to measure the effects of both extracellular and intracellular chloride on the deactivation of glycine and GABA currents at both negative and positive holding potentials. (ox.ac.uk)
- GABA A α5 inverse agonists) or elevate excitatory tone (e.g., glycine transporter inhibitors) offer novel approaches for treating diseases such as schizophrenia, AD and Down syndrome. (sri.com)
Rats1
- In this study WDR neuron behaviors in morphine tolerant rats and rats treated with GABA agonists, were recorded to elucidate the effect of morphine and GABA agonists on WDR behavioral changes. (ijabbr.com)
Amygdala1
- Based on the analysis of literature data, as well as our previous findings, we hypothesize that the level of GABA and, probably, its difference between the right and the left amygdala, may determine the differences in the anxiety levels in animals. (scirp.org)
Inhibitors1
- The main groups include sodium channel blockers, calcium current inhibitors, gamma-aminobutyric acid (GABA) enhancers, glutamate blockers, carbonic anhydrase inhibitors, hormones, and drugs with unknown mechanisms of action (see the image below). (medscape.com)
Brain4
- GABA is a chemical that is made in the brain. (amanitaresearch.com)
- GABA works by blocking brain signals (neurotransmissions). (amanitaresearch.com)
- in simple terms, GABA calms the CNS, reduces brain activity and eases bodily tension. (vagarights.com)
- It is different from GABA since it easily passes through the blood-brain barrier making it work faster. (consumerhealthdigest.com)
Anxiety3
- These findings suggest an important role in anxiety regulation of the amygdalar GABA levels, and the assumed GABA hemispheric lateralization. (scirp.org)
- GABA is taken for relieving anxiety, improving mood, reducing symptoms of PMS, and treating ADHD. (amanitaresearch.com)
- Again, it has an anxiolytic effect or the ability to relieve anxiety since it is a GABA agonist. (consumerhealthdigest.com)
Derivative2
- This medication is a derivative of gamma-aminobutyric acid (GABA), prescribed for severe chronic spasticity. (medindia.net)
- It is a derivative of GABA (gamma-aminobutyric acid). (consumerhealthdigest.com)
Hypnotics1
- The newer GABA-effective hypnotics are the only medications with demonstrated effectiveness in treating chronic insomnia with the majority of evidence supporting treatment efficacy for cognitive-behavioral therapy and short acting GABA-receptor agonists. (springer.com)
Nervous system2
- Besides the nervous system, GABA is also produced at relatively high levels in the insulin-producing β-cells of the pancreas. (amanitaresearch.com)
- Its selectivity for worms and similar invertebrates is because vertebrates only use GABA in the Central Nervous System and a worms GABA receptor is a different isoform to the vertebrate's one (Isoform: A protein having the same function and similar [or identical sequence], but the product of a different gene and usually). (americanaquariumproducts.com)
Dependence1
- The effect of GABA-positive agents on the formation of morphine dependence and on the manifestations of a withdrawal syndrome. (ijabbr.com)
Effects1
- Drugs that fall into this class exert their pharmacodynamic action by increasing the effects that an agonist has when potentiation is achieved. (wikipedia.org)
Synaptic1
- Using electrophysiological approaches, we showed that decreased reelin levels impair the maturation of GABAergic synaptic transmission without affecting the inhibitory nature of GABA. (frontiersin.org)
Alcohol2
- Alcohol is an indirect GABA agonist. (wikipedia.org)
- Sedative-hypnotic drugs are the primary agents for treatment of alcohol withdrawal syndrome because they are cross-tolerant drugs that modulate GABA functions. (medscape.com)
Drugs1
- Many commonly used sedative and anxiolytic drugs that affect the GABA receptor complex are not agonists. (wikipedia.org)
Tolerance1
- GABA is also used for increasing sense of well being, relieving injuries, improving exercise tolerance, decreasing body fat, and increasing lean body weight. (amanitaresearch.com)
Naturally1
- The test also found that the thyroid recovered naturally without further assistance after the Fluoride had been expelled by the GABA. (amanitaresearch.com)
Treatment1
- In treatment group, GABA agonists were injected on days 1, 3, 5 and 8 before injection of morphine. (ijabbr.com)
Pain1
- Results showed that chronic administration of morphine failed to attenuate formalin pain but GABA agonists improved analgesic effect of morphine. (ijabbr.com)