GABA Uptake Inhibitors
Nipecotic Acids
Neurotransmitter Uptake Inhibitors
GABA Plasma Membrane Transport Proteins
GABA Antagonists
Dopamine Uptake Inhibitors
Organic Anion Transporters
GABA Agonists
Benztropine
Membrane Transport Proteins
Nomifensine
Vigabatrin
Adrenergic Uptake Inhibitors
Receptors, GABA-A
Zimeldine
Baclofen
4-Aminobutyrate Transaminase
Synaptosomes
Serotonin Uptake Inhibitors
Muscimol
Desipramine
GABA Agents
Receptors, GABA-B
Isonicotinic Acids
GABA Modulators
Biological Transport
Serotonin
Oximes
Dose-Response Relationship, Drug
Rats, Sprague-Dawley
Cocaine
Carrier Proteins
Aminobutyrates
Clomipramine
beta-Alanine
Bicuculline
Dopamine
Dopamine Plasma Membrane Transport Proteins
Serotonin Antagonists
Neurons
Mazindol
Protriptyline
Metergoline
Fenfluramine
Quipazine
Amphetamines
GAT-3 transporters regulate inhibition in the neocortex. (1/32)
The role of GAT-3 transporters in regulating GABA(A) receptor-mediated inhibition was examined in the rat neocortex using an in vitro slice preparation. Pharmacologically isolated GABA(A) receptor-mediated responses were recorded from layer V neocortical pyramidal cells, and the effects of SNAP-5114, a GAT-3 GABA transporter-selective antagonist, were evaluated. Application of SNAP-5114 resulted in a reversible increase in the amplitude of an evoked GABA(A) response in most cells examined, although no effect on the decay time was observed. Examination of the spontaneous output of inhibitory interneurons revealed a reversible increase in the frequency and amplitude of spontaneous inhibitory synaptic currents as a consequence of GAT-3 inhibition. This effect of GAT-3 inhibition on spontaneous inhibitory events was action potential-dependent because no such increases were observed when SNAP-5114 was applied in the presence of TTX. These results demonstrate that GAT-3 transporters regulate inhibitory interneuron output in the neocortex. The increase in inhibitory interneuron excitability resulting from application of SNAP-5114 suggests that inhibition of GAT-3 transporter function results in a reduction in ambient GABA levels, possibly by a reduction in carrier-mediated GABA release via the GAT-3 transporter. (+info)Identification and selective inhibition of the channel mode of the neuronal GABA transporter 1. (2/32)
The function of GAT1, the transporter for the inhibitory neurotransmitter GABA, is characterized by expression in Xenopus laevis oocytes and measurements of GABA-induced uptake of [3H]GABA, 22Na+, and 36Cl-, and GABA-evoked currents under voltage-clamp conditions. N-[4,4-Diphenyl-3-butenyl]-nipecotic acid (SKF-89976-A), a specific inhibitor of GAT1, is used in our system as a pharmacological tool. The GABA-evoked current can be decomposed into a transport current, which is coupled to the GABA uptake, and a transmitter-gated current, which is uncoupled from the GABA uptake. The transport current results from a fixed stoichiometry of 1 GABA/2 Na+/1 Cl- transported during each cycle, as determined by radioactive tracer flux measurements. The transmitter-gated current is mediated by an Na+-conductance pathway. As a competitive inhibitor for GABA uptake, SKF-89976-A can separate the two current components. The GABA uptake is blocked with a K(I) value of approximately 7 microM, whereas the uncoupled transmitter-gated current is inhibited with a K(I) value of approximately 0.03 microM. Thus, the results of this study not only identify the transport mode and the channel mode of GAT1 but also raise the possibility of separating these components in a physiological environment. (+info)GABAergic signaling at mossy fiber synapses in neonatal rat hippocampus. (3/32)
In the adult rat hippocampus, granule cell mossy fibers (MFs) form excitatory glutamatergic synapses with CA3 principal cells and local inhibitory interneurons. However, evidence has been provided that, in young animals and after seizures, the same fibers can release in addition to glutamate GABA. Here we show that, during the first postnatal week, stimulation of granule cells in the dentate gyrus gave rise to monosynaptic GABAA-mediated responses in principal cells and in interneurons. These synapses were indeed made by MFs because they exhibited strong paired-pulse facilitation, high sensitivity to the metabotropic glutamate receptor agonist l-AP-4, and short-term frequency-dependent facilitation. MF responses were potentiated by blocking the plasma membrane GABA transporter GAT-1 with NO-711 or by allosterically modulating GABAA receptors with flurazepam. Chemical stimulation of granule cell dendrites with glutamate induced barrages of GABAA-mediated postsynaptic currents into target neurons. Furthermore, immunocytochemical experiments demonstrated colocalization of vesicular GABA transporter with vesicular glutamate transporter-1 and zinc transporter 3, suggesting that GABA can be taken up and stored in synaptic vesicles of MF terminals. Additional fibers releasing both glutamate and GABA into principal cells and interneurons were recruited by increasing the strength of stimulation. Both the GABAergic and the glutamatergic component of synaptic currents occurred with the same latency and were reversibly abolished by l-AP-4, indicating that they originated from the MFs. GABAergic signaling may play a crucial role in tuning hippocampal network during postnatal development. Low-threshold GABA-releasing fibers may undergo elimination, and this may occur when GABA shifts from the depolarizing to the hyperpolarizing direction. (+info)GABA transporters regulate a standing GABAC receptor-mediated current at a retinal presynaptic terminal. (4/32)
At the axon terminal of goldfish retinal bipolar cells, GABA(C) receptors have been shown to mediate inhibitory reciprocal synaptic currents. Here, we demonstrate a novel standing GABAergic current mediated exclusively by GABA(C) receptors. Selective inhibition of GAT-1 GABA transporters on amacrine cells increases this tonic current and reveals a specific functional coupling between GAT-1 transporters and GABA(C) receptors. We propose that this GABA(C) receptor-mediated standing current serves to regulate synaptic gain by shunting depolarizing potentials that can produce Ca2+-dependent action potentials at the bipolar cell terminal. Furthermore, we find that the amount of GABA(C) receptor-mediated reciprocal feedback between bipolar cell terminals and amacrine cells is greatly increased when GAT-1 transporters are specifically blocked by NO-711 (1-[2-[[(diphenylmethylene)imino]oxy]ethyl]-1,2,5,6-tetrahydro-3-pyridinecarboxyl ic acid hydrochloride). The involvement of GAT-1 transporters in regulating this standing (or tonic) GABA(C) current implicates them in a novel role as major determinants of presynaptic excitability. (+info)SNAP-25/syntaxin 1A complex functionally modulates neurotransmitter gamma-aminobutyric acid reuptake. (5/32)
Neurotransmitter gamma-aminobutyric acid (GABA) release to the synaptic clefts is mediated by the formation of a soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex, which includes two target SNAREs syntaxin 1A and SNAP-25 and one vesicle SNARE VAMP-2. The target SNAREs syntaxin 1A and SNAP-25 form a heterodimer, the putative intermediate of the SNARE complex. Neurotransmitter GABA clearance from synaptic clefts is carried out by the reuptake function of its transporters to terminate the postsynaptic signaling. Syntaxin 1A directly binds to the neuronal GABA transporter GAT-1 and inhibits its reuptake function. However, whether other SNARE proteins or SNARE complex regulates GABA reuptake remains unknown. Here we demonstrate that SNAP-25 efficiently inhibits GAT-1 reuptake function in the presence of syntaxin 1A. This inhibition depends on SNAP-25/syntaxin 1A complex formation. The H3 domain of syntaxin 1A is identified as the binding sites for both SNAP-25 and GAT-1. SNAP-25 binding to syntaxin 1A greatly potentiates the physical interaction of syntaxin 1A with GAT-1 and significantly enhances the syntaxin 1A-mediated inhibition of GAT-1 reuptake function. Furthermore, nitric oxide, which promotes SNAP-25 binding to syntaxin 1A to form the SNARE complex, also potentiates the interaction of syntaxin 1A with GAT-1 and suppresses GABA reuptake by GAT-1. Thus our findings delineate a further molecular mechanism for the regulation of GABA reuptake by a target SNARE complex and suggest a direct coordination between GABA release and reuptake. (+info)In the developing rat hippocampus a tonic GABAA-mediated conductance selectively enhances the glutamatergic drive of principal cells. (6/32)
In the adult hippocampus, two different forms of GABA(A) receptor-mediated inhibition have been identified: phasic and tonic. The first is due to the activation of GABA(A) receptors facing the presynaptic releasing sites, whereas the second is due to the activation of receptors localized away from the synapses. Because of their high affinity and low desensitization rate, extrasynaptic receptors are persistently able to sense low concentrations of GABA. Here we show that, early in postnatal life, between postnatal day (P) 2 and P6, CA1 and CA3 pyramidal cells but not stratum radiatum interneurons, express a tonic GABA(A)-mediated conductance. Block of the neuronal GABA transporter GAT-1 slightly enhanced the persistent GABA conductance in principal cells but not in GABAergic interneurons. However, in adulthood, a tonic GABA(A)-mediated conductance could be revealed in stratum radiatum interneurons, indicating that the ability of these cells to sense ambient GABA levels is developmentally regulated. Pharmacological analysis of the tonic conductance in principal cells demonstrated the involvement of beta2/beta 3, alpha 5 and gamma 2 GABA(A) receptor subunits. Removal of the tonic depolarizing action of GABA with picrotoxin, reduced the excitability and the glutamatergic drive of principal cells but did not modify the excitability of stratum radiatum interneurons. The increased cell excitability and synaptic activity following the activation of extrasynaptic GABA(A) receptors by ambient GABA would facilitate the induction of giant depolarizing potentials. (+info)Cloning and characterization of a functional human gamma-aminobutyric acid (GABA) transporter, human GAT-2. (7/32)
Plasma membrane gamma-aminobutyric acid (GABA) transporters act to terminate GABA neurotransmission in the mammalian brain. Intriguingly four distinct GABA transporters have been cloned from rat and mouse, whereas only three functional homologs of these transporters have been cloned from human. The aim of this study therefore was to search for this fourth missing human transporter. Using a bioinformatics approach, we successfully identified and cloned the full-length cDNA of a so far uncharacterized human GABA transporter (GAT). The predicted protein displays high sequence similarity to rat GAT-2 and mouse GAT3, and in accordance with the nomenclature for rat GABA transporters, we therefore refer to the transporter as human GAT-2. We used electrophysiological and cell-based methods to demonstrate that this protein is a functional transporter of GABA. The transport was saturable and dependent on both Na(+) and Cl(-). Pharmacologically the transporter is distinct from the other human GABA transporters and similar to rat GAT-2 and mouse GAT3 with high sensitivity toward GABA and beta-alanine. Furthermore the GABA transport inhibitor (S)-SNAP-5114 displayed some inhibitory activity at the transporter. Expression analysis by reverse transcription-PCR showed that GAT-2 mRNA is present in human brain, kidney, lung, and testis. The finding of the human GAT-2 demonstrates for the first time that the four plasma membrane GABA transporters identified in several mammalian species are all conserved in human. Furthermore the availability of human GAT-2 enables the use of all human clones of the GABA transporters in drug development programs and functional characterization of novel inhibitors of GABA transport. (+info)Nonvesicular inhibitory neurotransmission via reversal of the GABA transporter GAT-1. (8/32)
GABA transporters play an important but poorly understood role in neuronal inhibition. They can reverse, but this is widely thought to occur only under pathological conditions. Here we use a heterologous expression system to show that the reversal potential of GAT-1 under physiologically relevant conditions is near the normal resting potential of neurons and that reversal can occur rapidly enough to release GABA during simulated action potentials. We then use paired recordings from cultured hippocampal neurons and show that GABAergic transmission is not prevented by four methods widely used to block vesicular release. This nonvesicular neurotransmission was potently blocked by GAT-1 antagonists and was enhanced by agents that increase cytosolic [GABA] or [Na(+)] (which would increase GAT-1 reversal). We conclude that GAT-1 regulates tonic inhibition by clamping ambient [GABA] at a level high enough to activate high-affinity GABA(A) receptors and that transporter-mediated GABA release can contribute to phasic inhibition. (+info)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.
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.
Neurotransmitter uptake inhibitors are a class of drugs that work by blocking the reuptake of neurotransmitters, such as serotonin, norepinephrine, and dopamine, into the presynaptic neuron after they have been released into the synapse. This results in an increased concentration of these neurotransmitters in the synapse, which can enhance their signal transduction and lead to therapeutic effects.
These drugs are commonly used in the treatment of various psychiatric disorders, such as depression, anxiety, and attention deficit hyperactivity disorder (ADHD). They include selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and norepinephrine reuptake inhibitors (NRIs).
It's important to note that while neurotransmitter uptake inhibitors can be effective in treating certain conditions, they may also have potential side effects and risks. Therefore, it is essential to use them under the guidance and supervision of a healthcare professional.
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 (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.
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.
Dopamine uptake inhibitors are a class of medications that work by blocking the reuptake of dopamine, a neurotransmitter, into the presynaptic neuron. This results in an increased concentration of dopamine in the synapse, leading to enhanced dopaminergic transmission and activity.
These drugs are used in various medical conditions where dopamine is implicated, such as depression, attention deficit hyperactivity disorder (ADHD), and neurological disorders like Parkinson's disease. They can also be used to treat substance abuse disorders, such as cocaine addiction, by blocking the reuptake of dopamine and reducing the rewarding effects of the drug.
Examples of dopamine uptake inhibitors include:
* Bupropion (Wellbutrin), which is used to treat depression and ADHD
* Methylphenidate (Ritalin, Concerta), which is used to treat ADHD
* Amantadine (Symmetrel), which is used to treat Parkinson's disease and also has antiviral properties.
It's important to note that dopamine uptake inhibitors can have side effects, including increased heart rate, blood pressure, and anxiety. They may also have the potential for abuse and dependence, particularly in individuals with a history of substance abuse. Therefore, these medications should be used under the close supervision of a healthcare provider.
Organic anion transporters (OATs) are membrane transport proteins that are responsible for the cellular uptake and excretion of various organic anions, such as drugs, toxins, and endogenous metabolites. They are found in various tissues, including the kidney, liver, and brain, where they play important roles in the elimination and detoxification of xenobiotics and endogenous compounds.
In the kidney, OATs are located in the basolateral membrane of renal tubular epithelial cells and mediate the uptake of organic anions from the blood into the cells. From there, the anions can be further transported into the urine by other transporters located in the apical membrane. In the liver, OATs are expressed in the sinusoidal membrane of hepatocytes and facilitate the uptake of organic anions from the blood into the liver cells for metabolism and excretion.
There are several isoforms of OATs that have been identified, each with distinct substrate specificities and tissue distributions. Mutations in OAT genes can lead to various diseases, including renal tubular acidosis, hypercalciuria, and drug toxicity. Therefore, understanding the function and regulation of OATs is important for developing strategies to improve drug delivery and reduce adverse drug reactions.
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.
Benztropine is an anticholinergic medication that is primarily used to treat the symptoms of Parkinson's disease, such as rigidity, tremors, and muscle spasms. It works by blocking the action of acetylcholine, a neurotransmitter in the brain that is involved in the regulation of motor function.
Benztropine is also used to treat side effects caused by certain medications, such as antipsychotics, that can cause Parkinson-like symptoms. It may be prescribed to help reduce drooling or to manage muscle stiffness and restlessness.
The medication comes in the form of tablets or a solution for injection and is typically taken orally once or twice a day. Common side effects of benztropine include dry mouth, blurred vision, dizziness, and constipation. More serious side effects may include hallucinations, confusion, and irregular heartbeat.
It's important to note that benztropine can interact with other medications, so it's essential to inform your healthcare provider of all the drugs you are taking before starting this medication. Additionally, benztropine should be used cautiously in older adults, people with glaucoma or enlarged prostate, and those with a history of heart problems.
Membrane transport proteins are specialized biological molecules, specifically integral membrane proteins, that facilitate the movement of various substances across the lipid bilayer of cell membranes. They are responsible for the selective and regulated transport of ions, sugars, amino acids, nucleotides, and other molecules into and out of cells, as well as within different cellular compartments. These proteins can be categorized into two main types: channels and carriers (or pumps). Channels provide a passive transport mechanism, allowing ions or small molecules to move down their electrochemical gradient, while carriers actively transport substances against their concentration gradient, requiring energy usually in the form of ATP. Membrane transport proteins play a crucial role in maintaining cell homeostasis, signaling processes, and many other physiological functions.
Nomifensine is a medication that was previously used in the treatment of depression, but it is no longer available in many countries due to safety concerns. It is a non-tricyclic antidepressant that works by inhibiting the reuptake of dopamine and noradrenaline, which helps to increase the levels of these neurotransmitters in the brain and improve mood.
The medical definition of Nomifensine is:
"Nomifensine is a non-tricyclic antidepressant that is a potent inhibitor of dopamine and noradrenaline reuptake, with minimal effects on serotonin reuptake. It was used in the treatment of depression but has been withdrawn from the market due to safety concerns."
It's important to note that Nomifensine should only be taken under the supervision of a medical professional, and it is not available in many countries due to its potential for causing serious side effects such as liver toxicity and the risk of developing a rare but potentially fatal condition called hemolytic anemia.
Vigabatrin is an anticonvulsant medication used to treat certain types of seizures in adults and children. It works by reducing the abnormal excitement in the brain. The medical definition of Vigabatrin is: a irreversible inhibitor of GABA transaminase, which results in increased levels of gamma-aminobutyric acid (GABA) in the central nervous system. This medication is used as an adjunctive treatment for complex partial seizures and is available in oral form for administration.
It's important to note that Vigabatrin can cause serious side effects, including permanent vision loss, and its use should be closely monitored by a healthcare professional. It is also classified as a pregnancy category C medication, which means it may harm an unborn baby and should only be used during pregnancy if the potential benefit justifies the potential risk to the fetus.
Adrenergic uptake inhibitors are a class of medications that work by blocking the reuptake of neurotransmitters, such as norepinephrine and dopamine, into the presynaptic neuron. This results in an increase in the amount of neurotransmitter available to bind to postsynaptic receptors, leading to an enhancement of adrenergic transmission.
These medications are used in the treatment of various medical conditions, including depression, attention deficit hyperactivity disorder (ADHD), and narcolepsy. Some examples of adrenergic uptake inhibitors include:
* Tricyclic antidepressants (TCAs): These medications, such as imipramine and amitriptyline, were developed in the 1950s and are used to treat depression, anxiety disorders, and chronic pain.
* Selective serotonin-norepinephrine reuptake inhibitors (SNRIs): These medications, such as venlafaxine and duloxetine, were developed in the 1990s and are used to treat depression, anxiety disorders, and chronic pain.
* Norepinephrine-dopamine reuptake inhibitors (NDRIs): These medications, such as bupropion, are used to treat depression and ADHD.
It's important to note that these medications can have side effects and should be used under the supervision of a healthcare provider.
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.
Zimeldine is not commonly used in current medical practice due to its association with serious side effects. However, historically, it was a medication used as an antidepressant. It belongs to the class of drugs called selective serotonin reuptake inhibitors (SSRIs), which work by increasing the levels of the neurotransmitter serotonin in the brain.
Zimeldine was first synthesized in 1972 and approved for medical use in Sweden in 1982. However, it was withdrawn from the market in 1983 due to its association with a rare but serious side effect called Guillain-Barré syndrome, which is a neurological disorder that can cause muscle weakness and paralysis.
Although Zimeldine is no longer used in medical practice, it played an important role in the development of SSRIs as a class of antidepressants, which have since become widely used due to their effectiveness and relatively favorable side effect profile compared to earlier classes of antidepressants.
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.
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.
Synaptosomes are subcellular structures that can be isolated from the brain tissue. They are formed during the fractionation process of brain homogenates and consist of intact presynaptic terminals, including the synaptic vesicles, mitochondria, and cytoskeletal elements. Synaptosomes are often used in neuroscience research to study the biochemical properties and functions of neuronal synapses, such as neurotransmitter release, uptake, and metabolism.
Serotonin uptake inhibitors (also known as Selective Serotonin Reuptake Inhibitors or SSRIs) are a class of medications primarily used to treat depression and anxiety disorders. They work by increasing the levels of serotonin, a neurotransmitter in the brain that helps regulate mood, appetite, and sleep, among other functions.
SSRIs block the reuptake of serotonin into the presynaptic neuron, allowing more serotonin to be available in the synapse (the space between two neurons) for binding to postsynaptic receptors. This results in increased serotonergic neurotransmission and improved mood regulation.
Examples of SSRIs include fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), citalopram (Celexa), and escitalopram (Lexapro). These medications are generally well-tolerated, with side effects that may include nausea, headache, insomnia, sexual dysfunction, and increased anxiety or agitation. However, they can have serious interactions with other medications, so it is important to inform your healthcare provider of all medications you are taking before starting an SSRI.
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.
Desipramine is a tricyclic antidepressant (TCA) that is primarily used to treat depression. It works by increasing the levels of certain neurotransmitters, such as norepinephrine and serotonin, in the brain. These neurotransmitters are important for maintaining mood, emotion, and behavior.
Desipramine is also sometimes used off-label to treat other conditions, such as anxiety disorders, chronic pain, and attention deficit hyperactivity disorder (ADHD). It is available in oral form and is typically taken one to three times a day.
Like all medications, desipramine can cause side effects, which can include dry mouth, blurred vision, constipation, dizziness, and drowsiness. More serious side effects are rare but can include heart rhythm problems, seizures, and increased suicidal thoughts or behavior in some people, particularly children and adolescents.
It is important to take desipramine exactly as prescribed by a healthcare provider and to report any bothersome or unusual symptoms promptly. Regular follow-up appointments with a healthcare provider are also recommended to monitor the effectiveness and safety of the medication.
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.
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.
Isonicotinic acids are a group of chemical compounds that are structurally similar to nicotinic acid (also known as vitamin B3 or niacin). The term "isonicotinic" refers to the fact that these acids have a carboxylic acid group (-COOH) in the same position as the pyridine nitrogen atom in isonicotinic acid, which is a derivative of nicotinic acid.
Isonicotinic acids do not have a specific medical definition, but they may be used in various chemical and pharmaceutical applications. For example, isonicotinic acid hydrazide (also known as isoniazid) is an important anti-tuberculosis drug that has been widely used for many years.
It's worth noting that nicotinic acid and its derivatives have important medical uses as well, particularly in the treatment of pellagra, a disease caused by niacin deficiency. However, isonicotic acids are not typically associated with these medical applications.
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.
Biological transport refers to the movement of molecules, ions, or solutes across biological membranes or through cells in living organisms. This process is essential for maintaining homeostasis, regulating cellular functions, and enabling communication between cells. There are two main types of biological transport: passive transport and active transport.
Passive transport does not require the input of energy and includes:
1. Diffusion: The random movement of molecules from an area of high concentration to an area of low concentration until equilibrium is reached.
2. Osmosis: The diffusion of solvent molecules (usually water) across a semi-permeable membrane from an area of lower solute concentration to an area of higher solute concentration.
3. Facilitated diffusion: The assisted passage of polar or charged substances through protein channels or carriers in the cell membrane, which increases the rate of diffusion without consuming energy.
Active transport requires the input of energy (in the form of ATP) and includes:
1. Primary active transport: The direct use of ATP to move molecules against their concentration gradient, often driven by specific transport proteins called pumps.
2. Secondary active transport: The coupling of the movement of one substance down its electrochemical gradient with the uphill transport of another substance, mediated by a shared transport protein. This process is also known as co-transport or counter-transport.
Serotonin, also known as 5-hydroxytryptamine (5-HT), is a monoamine neurotransmitter that is found primarily in the gastrointestinal (GI) tract, blood platelets, and the central nervous system (CNS) of humans and other animals. It is produced by the conversion of the amino acid tryptophan to 5-hydroxytryptophan (5-HTP), and then to serotonin.
In the CNS, serotonin plays a role in regulating mood, appetite, sleep, memory, learning, and behavior, among other functions. It also acts as a vasoconstrictor, helping to regulate blood flow and blood pressure. In the GI tract, it is involved in peristalsis, the contraction and relaxation of muscles that moves food through the digestive system.
Serotonin is synthesized and stored in serotonergic neurons, which are nerve cells that use serotonin as their primary neurotransmitter. These neurons are found throughout the brain and spinal cord, and they communicate with other neurons by releasing serotonin into the synapse, the small gap between two neurons.
Abnormal levels of serotonin have been linked to a variety of disorders, including depression, anxiety, schizophrenia, and migraines. Medications that affect serotonin levels, such as selective serotonin reuptake inhibitors (SSRIs), are commonly used to treat these conditions.
Oximes are a class of chemical compounds that contain the functional group =N-O-, where two organic groups are attached to the nitrogen atom. In a clinical context, oximes are used as antidotes for nerve agent and pesticide poisoning. The most commonly used oxime in medicine is pralidoxime (2-PAM), which is used to reactivate acetylcholinesterase that has been inhibited by organophosphorus compounds, such as nerve agents and certain pesticides. These compounds work by forming a bond with the phosphoryl group of the inhibited enzyme, allowing for its reactivation and restoration of normal neuromuscular function.
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.
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.
Cocaine is a highly addictive stimulant drug derived from the leaves of the coca plant (Erythroxylon coca). It is a powerful central nervous system stimulant that affects the brain and body in many ways. When used recreationally, cocaine can produce feelings of euphoria, increased energy, and mental alertness; however, it can also cause serious negative consequences, including addiction, cardiovascular problems, seizures, and death.
Cocaine works by increasing the levels of dopamine in the brain, a neurotransmitter associated with pleasure and reward. This leads to the pleasurable effects that users seek when they take the drug. However, cocaine also interferes with the normal functioning of the brain's reward system, making it difficult for users to experience pleasure from natural rewards like food or social interactions.
Cocaine can be taken in several forms, including powdered form (which is usually snorted), freebase (a purer form that is often smoked), and crack cocaine (a solid form that is typically heated and smoked). Each form of cocaine has different risks and potential harms associated with its use.
Long-term use of cocaine can lead to a number of negative health consequences, including addiction, heart problems, malnutrition, respiratory issues, and mental health disorders like depression or anxiety. It is important to seek help if you or someone you know is struggling with cocaine use or addiction.
Carrier proteins, also known as transport proteins, are a type of protein that facilitates the movement of molecules across cell membranes. They are responsible for the selective and active transport of ions, sugars, amino acids, and other molecules from one side of the membrane to the other, against their concentration gradient. This process requires energy, usually in the form of ATP (adenosine triphosphate).
Carrier proteins have a specific binding site for the molecule they transport, and undergo conformational changes upon binding, which allows them to move the molecule across the membrane. Once the molecule has been transported, the carrier protein returns to its original conformation, ready to bind and transport another molecule.
Carrier proteins play a crucial role in maintaining the balance of ions and other molecules inside and outside of cells, and are essential for many physiological processes, including nerve impulse transmission, muscle contraction, and nutrient uptake.
Aminobutyrates are compounds that contain an amino group (-NH2) and a butyric acid group (-CH2-CH2-CH2-COOH). The most common aminobutyrate is gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter in the central nervous system. GABA plays a crucial role in regulating brain excitability and is involved in various physiological processes, including sleep, memory, and anxiety regulation. Abnormalities in GABAergic neurotransmission have been implicated in several neurological and psychiatric disorders, such as epilepsy, anxiety disorders, and chronic pain. Other aminobutyrates may also have important biological functions, but their roles are less well understood than that of GABA.
Clomipramine is a tricyclic antidepressant drug that is primarily used to treat obsessive-compulsive disorder (OCD). It works by increasing the levels of certain neurotransmitters, such as serotonin and norepinephrine, in the brain. These neurotransmitters are involved in regulating mood and behavior.
Clomipramine is also used off-label to treat other conditions, including panic disorder, depression, chronic pain, and sleep disorders. It is available as a tablet or capsule and is typically taken one to three times a day. Common side effects of clomipramine include dry mouth, constipation, blurred vision, dizziness, and drowsiness.
As with all medications, clomipramine should be used under the close supervision of a healthcare provider, who can monitor its effectiveness and potential side effects. It is important to follow the dosage instructions carefully and to report any unusual symptoms or concerns to the healthcare provider promptly.
Beta-alanine is a non-essential amino acid, which means that it is not required in the diet because the body can produce it from other amino acids. It is produced in the liver and is also found in some foods such as meat, poultry, and fish.
Beta-alanine plays a role in the production of carnosine, a dipeptide molecule that helps to regulate muscle pH and improve muscle function during high-intensity exercise. When muscles contract during intense exercise, they produce hydrogen ions, which can cause the muscle pH to decrease (become more acidic), leading to fatigue and reduced muscle function. Carnosine acts as a buffer against this acidity, helping to maintain optimal muscle pH levels and improve performance during high-intensity exercise.
Beta-alanine supplements have been shown to increase carnosine levels in muscles, which may lead to improved athletic performance, particularly in activities that require short bursts of intense effort, such as weightlifting or sprinting. However, more research is needed to fully understand the effects and potential benefits of beta-alanine supplementation.
It's important to note that while beta-alanine supplements are generally considered safe for most people, they can cause a tingling sensation in the skin (paresthesia) when taken in high doses. This is a harmless side effect and typically subsides within an hour or so of taking the supplement.
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.
Dopamine is a type of neurotransmitter, which is a chemical messenger that transmits signals in the brain and nervous system. It plays several important roles in the body, including:
* Regulation of movement and coordination
* Modulation of mood and motivation
* Control of the reward and pleasure centers of the brain
* Regulation of muscle tone
* Involvement in memory and attention
Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area. It is released by neurons (nerve cells) and binds to specific receptors on other neurons, where it can either excite or inhibit their activity.
Abnormalities in dopamine signaling have been implicated in several neurological and psychiatric conditions, including Parkinson's disease, schizophrenia, and addiction.
Dopamine plasma membrane transport proteins, also known as dopamine transporters (DAT), are a type of protein found in the cell membrane that play a crucial role in the regulation of dopamine neurotransmission. They are responsible for the reuptake of dopamine from the synaptic cleft back into the presynaptic neuron, thereby terminating the signal transduction of dopamine and regulating the amount of dopamine available for further release.
Dopamine transporters belong to the family of sodium-dependent neurotransmitter transporters and are encoded by the SLC6A3 gene in humans. Abnormalities in dopamine transporter function have been implicated in several neurological and psychiatric disorders, including Parkinson's disease, attention deficit hyperactivity disorder (ADHD), and substance use disorders.
In summary, dopamine plasma membrane transport proteins are essential for the regulation of dopamine neurotransmission by mediating the reuptake of dopamine from the synaptic cleft back into the presynaptic neuron.
Serotonin antagonists are a class of drugs that block the action of serotonin, a neurotransmitter, at specific receptor sites in the brain and elsewhere in the body. They work by binding to the serotonin receptors without activating them, thereby preventing the natural serotonin from binding and transmitting signals.
Serotonin antagonists are used in the treatment of various conditions such as psychiatric disorders, migraines, and nausea and vomiting associated with cancer chemotherapy. They can have varying degrees of affinity for different types of serotonin receptors (e.g., 5-HT2A, 5-HT3, etc.), which contributes to their specific therapeutic effects and side effect profiles.
Examples of serotonin antagonists include ondansetron (used to treat nausea and vomiting), risperidone and olanzapine (used to treat psychiatric disorders), and methysergide (used to prevent migraines). It's important to note that these medications should be used under the supervision of a healthcare provider, as they can have potential risks and interactions with other drugs.
Tropane alkaloids are a class of naturally occurring compounds that contain a tropane ring in their chemical structure. This ring is composed of a seven-membered ring with two nitrogen atoms, one of which is part of a piperidine ring. Tropane alkaloids are found in various plants, particularly those in the Solanaceae family, which includes nightshade, belladonna, and datura. Some well-known tropane alkaloids include atropine, scopolamine, and cocaine. These compounds have diverse pharmacological activities, such as anticholinergic, local anesthetic, and central nervous system stimulant effects.
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.
Mazindol is a prescription medication that belongs to a class of drugs known as sympathomimetic amines or anorectics. It has been used in the treatment of obesity, as it works by reducing appetite and increasing the amount of energy that the body uses. Mazindol affects certain chemicals in the brain that control appetite.
It's important to note that mazindol is not commonly used today due to its potential for abuse and serious side effects. It should only be used under the close supervision of a healthcare provider, and its use is typically reserved for individuals with severe obesity who have not responded to other treatment options.
Protriptyline is a tricyclic antidepressant (TCA) medication. It is primarily used to treat symptoms of depression, but it can also be used for other conditions such as anxiety disorders or to help manage chronic pain. Protriptyline works by increasing the levels of certain neurotransmitters in the brain, such as norepinephrine and serotonin, which can help to improve mood and reduce symptoms of depression.
Protriptyline has a sedating effect, so it may also be used to treat insomnia or agitation associated with depression. It is available in immediate-release tablet form and is typically taken two to four times per day. As with all medications, protriptyline can have side effects, including dry mouth, blurred vision, constipation, and dizziness. It may also cause cardiac arrhythmias and should be used with caution in patients with a history of heart disease.
It's important to note that the use of Protriptyline and other tricyclic antidepressants has declined over the years due to the development of newer classes of antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), which have fewer side effects and are safer in overdose. However, protriptyline may still be prescribed in certain cases where other treatments have not been effective.
Methysergide, commonly known as methylergometrine or metergoline, is not typically considered a medication in the medical field. It is actually a derivative of ergot alkaloids, which are fungal metabolites that have been used in medicine for their vasoconstrictive and oxytocic properties.
Methysergide has been used in the past as a migraine prophylaxis medication due to its ability to block serotonin receptors in the brain. However, its use is now limited due to its potential to cause serious side effects such as fibrotic reactions in various organs, including the heart, lungs, and kidneys.
Therefore, methysergide/metergoline is not commonly used in modern medical practice, and its use is typically reserved for highly specific cases under close medical supervision.
Pargyline is an antihypertensive drug and a irreversible monoamine oxidase inhibitor (MAOI) of type B. It works by blocking the breakdown of certain chemicals in the brain, such as neurotransmitters, which can help improve mood and behavior in people with depression.
Pargyline is not commonly used as a first-line treatment for depression due to its potential for serious side effects, including interactions with certain foods and medications that can lead to dangerously high blood pressure. It is also associated with a risk of serotonin syndrome when taken with selective serotonin reuptake inhibitors (SSRIs) or other drugs that increase serotonin levels in the brain.
Pargyline is available only through a prescription and should be used under the close supervision of a healthcare provider.
Anticonvulsants are a class of drugs used primarily to treat seizure disorders, also known as epilepsy. These medications work by reducing the abnormal electrical activity in the brain that leads to seizures. In addition to their use in treating epilepsy, anticonvulsants are sometimes also prescribed for other conditions, such as neuropathic pain, bipolar disorder, and migraine headaches.
Anticonvulsants can work in different ways to reduce seizure activity. Some medications, such as phenytoin and carbamazepine, work by blocking sodium channels in the brain, which helps to stabilize nerve cell membranes and prevent excessive electrical activity. Other medications, such as valproic acid and gabapentin, increase the levels of a neurotransmitter called gamma-aminobutyric acid (GABA) in the brain, which has a calming effect on nerve cells and helps to reduce seizure activity.
While anticonvulsants are generally effective at reducing seizure frequency and severity, they can also have side effects, such as dizziness, drowsiness, and gastrointestinal symptoms. In some cases, these side effects may be managed by adjusting the dosage or switching to a different medication. It is important for individuals taking anticonvulsants to work closely with their healthcare provider to monitor their response to the medication and make any necessary adjustments.
Fenfluramine is a drug that was previously used for the short-term treatment of obesity. It works by suppressing appetite and increasing the feeling of fullness. Fenfluramine is an amphetamine derivative and stimulates the release of serotonin, a neurotransmitter in the brain that helps regulate mood, appetite, and sleep.
Fenfluramine was commonly prescribed in combination with phentermine, another appetite suppressant, under the brand name Fen-Phen. However, in 1997, the U.S. Food and Drug Administration (FDA) issued a public health warning about the potential risk of serious heart valve damage associated with the use of fenfluramine and withdrew its approval for the drug's use. Since then, fenfluramine has not been approved for medical use in many countries, including the United States.
Quipazine is not generally considered a medical term, but it is a chemical compound that has been studied in the field of medicine and neuroscience. Quipazine is a type of drug known as a serotonin receptor agonist, which means it binds to and activates serotonin receptors in the brain.
Serotonin is a neurotransmitter, a chemical that transmits signals in the brain and nervous system, that plays a role in regulating mood, appetite, sleep, and other functions. Quipazine has been studied for its potential therapeutic uses in various conditions, including depression, anxiety, schizophrenia, and substance abuse disorders. However, it is not currently approved for use as a medication in any country.
It's important to note that while quipazine may have potential therapeutic benefits, it also has significant side effects, including seizures, changes in heart rate and blood pressure, and neuroleptic malignant syndrome, a potentially life-threatening condition characterized by muscle rigidity, fever, and autonomic dysfunction. As such, its use is generally limited to research settings.
Amphetamines are a type of central nervous system stimulant drug that increases alertness, wakefulness, and energy levels. They work by increasing the activity of certain neurotransmitters (chemical messengers) in the brain, such as dopamine and norepinephrine. Amphetamines can be prescribed for medical conditions such as attention deficit hyperactivity disorder (ADHD) and narcolepsy, but they are also commonly abused for their ability to produce euphoria, increase confidence, and improve performance in tasks that require sustained attention.
Some common examples of amphetamines include:
* Adderall: a combination of amphetamine and dextroamphetamine, used to treat ADHD and narcolepsy
* Dexedrine: a brand name for dextroamphetamine, used to treat ADHD and narcolepsy
* Vyvanse: a long-acting formulation of lisdexamfetamine, a prodrug that is converted to dextroamphetamine in the body, used to treat ADHD
Amphetamines can be taken orally, snorted, smoked, or injected. Long-term use or abuse of amphetamines can lead to a number of negative health consequences, including addiction, cardiovascular problems, malnutrition, mental health disorders, and memory loss.
"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.
Tiagabine
Arecaidine
CI-966
Nipecotic acid
Gabaculine
GABA transporter type 3
Isoguvacine
GABA reuptake inhibitor
C6H11NO2
Morphine-3-glucuronide
Vesicular monoamine transporter 2
NNC-711
Guvacine
Monoamine transporter
Duloxetine
DOV Pharmaceutical
Diazepam
List of MeSH codes (D27)
Deramciclane
Valproate
Reuptake inhibitor
Anxiolytic
Neurotransmitter transporter
Neuropharmacology
Clonazepam
Central nervous system fatigue
Pipofezine
Lithium (medication)
Tedral
Neuromodulation
Tiagabine - Wikipedia
Antiepileptic Drugs: Overview, Mechanism of Action, Sodium Channel Blockers
Erowid.org: Erowid Reference 7234 : Inhibitors of synaptosomal gamma-hydroxybutyrate transport : McCormick SJ, Tunnicliff G
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Receptors12
- The natural products magnolol and honokiol are positive allosteric modulators of both synaptic and extra-synaptic GABA(A) receptors. (musc.edu)
- RNA editing of the GABA(A) receptor alpha3 subunit alters the functional properties of recombinant receptors. (musc.edu)
- Non-selective benzodiazepine (BZ) binding-site full agonists, exemplified by diazepam, act by enhancing the inhibitory effects of GABA at GABA(A) receptors containing either an alpha1, -2, -3 or -5 subunit. (hhs.gov)
- More specifically, the alpha2- and/or alpha3-containing GABA(A) receptors play a role in anxiety whereas the alpha1 subtype is involved in sedation, raising the possibility of a compound that selectively modulates alpha2- and/or alpha3-containing receptors but does not affect alpha1-containing receptors would be a non-sedating anxiolytic. (hhs.gov)
- The benzodiazepine binding site of GABA(A) receptors as a target for the development of novel anxiolytics. (hhs.gov)
- 3 Synaptic terminals from local and distant γ-aminobutyric acid (GABA)-containing neurons 4,5 as well as GABA type A (GABA A ) receptors 6-8 are present in the pontine reticular formation and modulate behavioral arousal. (silverchair.com)
- CBG interacts with both the CB1 and CB2 receptors, acting as a possible inhibitor to the psychoactive effects of THC. (emeraldgardencbd.com)
- They are also present on the plasma membrane of neurons and glia which help define their function of regulation of GABA concentration as they act as the receptors that facilitate recycling of GABA in the extracellular space. (csnpharm.cn)
- g ami nobutyric acid receptors and the GABA uptake system are present in both male and female genital tract. (ainhibitor.com)
- Stiripentol is an antiepileptic drug that can inhibit the synaptosomal uptake of GABA, increase the activation of GABAA receptors, its also a microsomal cytochrome P450 (CYP) isoforms CYP3A4, CYP1A2, and CYP2C19 inhibitor. (csnpharm.com)
- GABA receptors are chlorine channels that mediate postsynaptic inhibition, resulting in postsynaptic neuron hyperpolarization. (medscape.com)
- Lewter is studying the behavioral effects of novel positive allosteric modulators (PAMS) for alpha-2 and alpha-3 containing GABA A receptors and the potential utility of these PAMs as analgesics. (buffalo.edu)
Inhibition8
- Moreover, the absence of inhibition by GABA uptake inhibitors shows that gamma-hydroxybutyrate transport is a separate entity from GABA transport. (erowid.org)
- Without a doubt, the inhibition of 5 HT synthesis GABA receptor by pCPA, which has previously been shown to provide marked 5 HT and 5 HIAA depletion in unique locations on the pigeon brain, might blunt the emesis induced by 5 HT, receptor antagonists. (gabasignaling.com)
- Contributes to GABA reuptake inhibition. (injoyextracts.com)
- Choline uptake was characterized by Na+-independence, a single-uptake mechanism, and inhibition by choline-uptake inhibitor HC-3, similar to the function of CTL1. (bvsalud.org)
- Most anesthetic drugs potentiate GABA A receptor-mediated inhibition, and this potentiation is thought to comprise part of the mechanism by which general anesthetics produce hypnosis. (silverchair.com)
- Role of T type VOCCs was further reinforced by inhibition of acrosome reaction mediated by human SIZP in presence Inhibitors,Modulators,Libraries of two different T type VOCCs inhibitors. (ainhibitor.com)
- The antidepressant, antiobsessive-compulsive, and antibulimic actions of citalopram are presumed to be linked to its inhibition of CNS neuronal uptake of serotonin. (illumina.com)
- Considered collectively, the findings demonstrate that LTP FC involves (1) elevation of [K + ] o in the DH s , (2) NMDAR activation, and (3) conversion of the effect of GABA on DH s neurons from inhibition to excitation. (en-journal.org)
Serotonin uptake inh1
- A furancarbonitrile that is one of the SEROTONIN UPTAKE INHIBITORS used as an antidepressant. (illumina.com)
Inhibits6
- CBG inhibits GABA uptake, which could lead to muscle relaxation, tension relief , and sensation of calm and peace in the body and brain. (injoyextracts.com)
- Picroto in a GABAA receptor inhibitor, inhibits pro gesterone as well as recombinant human ZP3 fragment mediated acrosome reaction. (ainhibitor.com)
- inhibits the generation of NADPH oxidase complex in the activation of respiratory burst of PMNs, but does not directly inhibit the activity of NADPH oxidase already generated, and is a non-selective cytochrome P450 inhibitor. (csnpharm.com)
- 3 St. John's Wort inhibits re-uptake of serotonin, dopamine, norepinephrine, and GABA, increasing their circulating availability for neural cells. (ivcjournal.com)
- We have a molecule called GABA which inhibits the electrical impulses, passionflower and lemon balm modulate this. (threespiritdrinks.com)
- The way it works is that valerenic acid works as a central nervous system (CNS) depressant, and also inhibits the enzymatic breakdown of GABA. (threespiritdrinks.com)
Neurons5
- Tiagabine is thought to block GABA uptake into presynaptic neurons as a result of this action, allowing more GABA to be available for receptor binding on the surfaces of post-synaptic cells. (wikipedia.org)
- This excitatory transmission is found to be GABAergic, which is demonstrated by the use of GABA antagonists, uptake inhibitors, and double-labeling experiments showing that Cr-Aint neurons are GABA-immunoreactive. (jneurosci.org)
- Magnetic resonance imaging volume reconstruction and immunofluorescence analysis of grafted cell survival showed near complete injury-cavity-filling by grafted cells and development of putative GABA-ergic synapses between grafted and host neurons. (biomedcentral.com)
- Whole-cell patch recordings were carried out to evaluate the effects of FC on the response of DH s neurons to puffer-applied GABA. (en-journal.org)
- Biphasic GABA A -mediated postsynaptic responses can be readily evoked in CA1 pyramidal neurons of rat hippocampal slices by high-frequency stimulus (HFS) trains in the presence of ionotropic glutamate receptor antagonists. (jneurosci.org)
Agonists2
- Yeah, and GABA agonists. (abovetopsecret.com)
- The discovery provided a potential mechanism to account for the widespread use of indirect-acting 5-HT receptor agonists - such as selective serotonin re-uptake inhibitors - in combination with opioids for treating pain. (buffalo.edu)
Reuptake6
- Tiagabine may be used alongside selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, or benzodiazepines for anxiety, or antidepressants, gabapentin, other anticonvulsants, or opioids for neuropathic pain. (wikipedia.org)
- Tiagabine increases the level of γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system, by blocking the GABA transporter 1 (GAT-1), and hence is classified as a GABA reuptake inhibitor (GRI). (wikipedia.org)
- Moreover, Gamma-aminobutyric acid (GABA)* reuptake is greater than THC or CBD, suggesting that CBG could possess muscle relaxant properties. (hemppedia.org)
- Citalopram is one of a class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs). (illumina.com)
- In vitro studies show that citalopram is a potent and selective inhibitor of neuronal serotonin reuptake and has only very weak effects on norepinephrine and dopamine neuronal reuptake. (illumina.com)
- St Johns wort works in the same way that popular pharmaceuticals selective serotonin reuptake inhibitors (SSRI's) work. (threespiritdrinks.com)
Inhibit3
- Consequently, several therapeutic agents such as adiponectin, ezetimibe, GABA tea, geniposide, liraglutide, guava extract, and vitamin D were shown to inhibit diabetes and its complications through modulation of the autophagy pathway. (frontiersin.org)
- In contrast to T type VOCCs inhibitors, L type VOCCs inhibitors failed to inhibit SIZP mediated acrosome reaction. (ainhibitor.com)
- SSRIs inhibit central nervous system (CNS) neuronal uptake of serotonin (5HT). (medscape.com)
Monoamine oxidase in1
- St. John's Wort should not be used with pharmacologic antidepressants that have similar mechanisms of action, such as monoamine oxidase inhibitors (MAOI), because of the risk for serotonin toxicity. (ivcjournal.com)
Synthesis1
- Each rat received microinjections of Ringer's (vehicle control), the GABA uptake inhibitor nipecotic acid, and the GABA synthesis inhibitor 3-mercaptopropionic acid. (silverchair.com)
Modulators4
- In this manuscript, we have identified Inhibitors,Modulators,Libraries type of VOCCs responsible for the early intra cellular calcium influ as well as their role in acrosomal e ocytosis mediated by SIZP in human sperm. (ainhibitor.com)
- A Inhibitors,Modulators,Libraries spe cific binding and transport system is present on the plasma membrane of the human spermatozoon. (ainhibitor.com)
- Out of two classified GABA receptor subtypes Inhibitors,Modulators,Libraries GABAA and GABAB, GABAA receptor is a plasma membrane multi subunit receptor comple linked to the chloride channel whose activation results in the opening of the chloride channel. (ainhibitor.com)
- Inhibitors,Modulators,Libraries 5 AW containing hydrosoluble components was obtained after the washing of the particle Inhibitors,Modulators,Libraries suspension and two cen trifugations at 10,000 Inhibitors,Modulators,Libraries g, followed by filtration of the super natant through a 0. (ainhibitor.com)
Dopamine6
- There was a dose- and calcium-dependent release of dopamine from turtle retinas incubated in $\sp3$H-dopamine after perfusion of the GABA antagonist bicuculline. (tmc.edu)
- This indicated that dopamine release was tonically inhibited by GABA. (tmc.edu)
- The cells capable of the release of dopamine were identified using both uptake autoradiography and immunocytochemical localization with dopamine antisera. (tmc.edu)
- It's the Tribulus Terrestris I guess - MAO inhibitors like that can stimulate, excite weird, probably dopamine pathways. (abovetopsecret.com)
- Many of these botanical remedies work by modulating neurotransmitters such as serotonin, dopamine, norepinephrine, and gamma-aminobutyric acid (GABA). (ivcjournal.com)
- Glutamate gets the brain excited and GABA calms the brain and then there are all these dimmer switches, which are serotonin, dopamine, acetylcholine, glycine, and all these other neurotransmitters. (drweitz.com)
Nipecotic2
- Four inhibitors of GABA transport - nipecotic acid, guvacine, ketamine and beta-alanine and GABA itself, were without effect on gamma-hydroxybutyrate transport. (erowid.org)
- Nipecotic acid is an inhibitor of GABA uptake with IC50 values of 8, 106 and 2370 mM for hGABA T-1, hGABA T-3 and hBGT-1 respectively. (csnpharm.cn)
Acid7
- Although the exact mechanism by which Tiagabine exerts its antiseizure effect is unknown, it is thought to be related to its ability to increase the activity of gamma aminobutyric acid (GABA), the central nervous system's major inhibitory neurotransmitter. (wikipedia.org)
- 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)
- Several gamma-hydroxybutyrate and gamma-aminobutyric acid (GABA) structural analogues were tested as potential inhibitors of gamma-hydroxybutyrate transport. (erowid.org)
- Many general anesthetics are thought to produce a loss of wakefulness, in part, by enhancing gamma-aminobutyric acid (GABA) neurotransmission. (silverchair.com)
- GABA is an amino acid, the primary neurotransmitter for the central nervous system. (hemppedia.org)
- GABA transporters (Gamma-Aminobutyric acid transporters) belong to the family of neurotransmitters known as sodium symporters, also known as solute carrier 6 (SLC6). (csnpharm.cn)
- Benzodiazepines bind to a specific receptor on the gamma amino-butyric acid (GABA) receptor complex, thereby increasing the affinity of GABA for its receptor. (medscape.com)
Competitive inhibitor2
- The most effective inhibitor was harmaline (Ki = 94 +/- 21 micromol/l), a known competitive inhibitor of Na+ binding to certain transport proteins. (erowid.org)
- Bergaptin is a competitive inhibitor of CYP1A1 with Ki of 10.7 nM. (csnpharm.com)
Antidepressants1
- The drug is also effective in reducing ethanol uptake in alcoholics and is used in depressed patients who also suffer from tardive dyskinesia in preference to tricyclic antidepressants, which aggravate this condition. (illumina.com)
Antagonist2
- The inability of locally infused GR127935 to enhance extracellular 5 HT concentration contrasts markedly together with the result of the non selective S HTm receptor antagonist, methiothepin, for which the boost was comparable in magnitude to PDK 1 Signaling that of the 5 HT re uptake inhibitor, fluoxetine. (gabasignaling.com)
- 9,10 Conversely, microinjecting the GABA A receptor antagonist bicuculline into the pontine reticular formation increases REM sleep and decreases wakefulness. (silverchair.com)
Analgesic1
- CBG is a strong Anandamide (AEA) uptake inhibitor and powerful agent against MRSA and displays analgesic and antidepressant properties. (hemppedia.org)
Transporter3
- Here, we examined molecular and functional analyses of choline transporters in human pancreatic-cancer cell line MIA PaCa-2 and the elucidation of the action mechanism behind the antitumor effect of novel choline-transporter-like protein 1 (CTL1) inhibitors, Amb4269951 and its derivative Amb4269675. (bvsalud.org)
- SKF-89976A HCl is a selective GABA transporter (GAT-1) inhibitor with IC50s of 0.28 μM, 137.34 μM and 202.8 μM for GAT-1, GAT-2 and GAT-3 in CHO cells, respectively. (csnpharm.cn)
- Guvacine hydrochloride, an alkaloid from the nut of Areca catechu, acts as an inhibitor of GABA transporter, and dispalys modest selectivity for cloned GABA transporters with IC50 values of 14 μM (human GAT-1), 39 μM (rat GAT-1), 58 μM (rat GAT-2), 119 μM (human GAT-3), 378 μM (rat GAT-3), and 1870 μM (human BGT-3). (csnpharm.cn)
IC504
- Mefentrifluconazole is a potent, selective and orally active fungal CYP51 (Kd= 0.5 nM) inhibitor, but shows less inhibitory activity on human aromatase (IC50=0.92 μM). (csnpharm.com)
- HET-0016 is a potent and selective inhibitor of the biosynthesis of 20-HETE in human renal microsomes with an IC50 of 8.9 nM, selectively inhibiting CYP4A and 4F isoforms. (csnpharm.com)
- HY-B0258), is a potent and competitive P450 (CYP) isoform CYP2C8 inhibitor with an IC50 of 4.07 μM[1][2]. (csnpharm.com)
- Furafylline is a potent and selective inhibitor of human cytochrome P450IA2 with IC50 of 0.07 μM. (csnpharm.com)
Potent2
- Dazoxiben hydrochloride is a potent, orally active thromboxane (TX) synthase inhibitor that reduces the formation of blood clots. (csnpharm.com)
- 6,7-Dihydroxybergamottin acetonide is a natural product isolated and purified from the peels of Citrus maxima, and is a potent inhibitor of CYP3A activity, being primarily responsible for the effects of grapefruit juice on cytochrome P450 activity in humans. (csnpharm.com)
Degradation1
- it is not converted metabolically into GABA or a GABA agonist and is not an inhibitor of GABA uptake or degradation. (medscape.com)
Synaptosomal1
- McCormick SJ, Tunnicliff G. "Inhibitors of synaptosomal gamma-hydroxybutyrate transport" Pharmacology . (erowid.org)
Extracellular3
- These results suggest that the uptake of extracellular choline in MIA PaCa-2 cells is mediated by CTL1. (bvsalud.org)
- These transporters are primarily responsible for the regulation of extracellular GABA concentration during basal and synaptic activity. (csnpharm.cn)
- The HFS train evoked a rapid GABA A -mediated bicarbonate-dependent increase in the extracellular K + concentration ([K + ] o ), and the GDPSP followed the K + transient in a sub-Nernstian manner. (jneurosci.org)
Antifungal1
- Dapaconazole,a CYP51 inhibitor is an antifungal drug candidate. (csnpharm.com)
Muscimol1
- For example, microinjecting the GABA A receptor agonist muscimol into the pontine reticular formation increases wakefulness. (silverchair.com)
Norepinephrine1
- Norepinephrine encourages focus and concentration, and GABA, also known as the "inhibitor transmitter", promotes a sense of calm. (ivcjournal.com)
GABAA1
- Studies presented in this manuscript suggest that in humans, ZP mediated induction of acrosome reaction is also inhibited by inhibitor of GABAA receptor. (ainhibitor.com)
Selectivity1
- The status of these and other BZ site compounds with claimed, but often not explicitly stated, GABA(A) subtype selectivity (such as ELB-139 and ocinaplon) will be reviewed in relation to their development as non-sedating anxiolytics for the treatment of generalised anxiety disorder. (hhs.gov)
Transporters2
- However, the molecular mechanisms of choline uptake and choline transporters in pancreatic cancer have not been elucidated. (bvsalud.org)
- GABA transporters often are the main sites that are aimed by lot of anticonvulsant drugs in order to avoid seizure disorders such as epilepsy. (csnpharm.cn)
Potentiate1
- Progesterone and its metabolites potentiate the effects of GABA on this receptor. (ainhibitor.com)
Excitatory1
- The excitatory GABA theory has been questioned as potentially being an artefact of experimental conditions. (gabasignaling.com)
Bilateral2
- For this, rats received bilateral microinjection of the choline uptake inhibitor hemicholinium-3 before exposure to restraint stress. (bvsalud.org)
- Uptake and efficacy of bilateral risk reducing surgery in unaffected female BRCA1 and BRCA2 carriers. (cdc.gov)
Anxiety2
- GABA uptake inhibitors are already used to treat anxiety. (injoyextracts.com)
- GABA uptake in the brain may be obstructed by CBG, making this cannabinoid a possible anti-anxiety agent and muscle relaxant. (emeraldgardencbd.com)
Enzyme1
- This agent is an enzyme inhibitor derived from processed red blood cells that is an iron-containing metalloporphyrin. (medscape.com)
Molecule1
- CTL1 is a target molecule for the treatment of pancreatic cancer, and its inhibitors Amb4269951 and Amb4269675 are novel lead compounds. (bvsalud.org)
Effects1
- However, the advent of molecular genetic and pharmacological approaches has begun to delineate which GABA(A) receptor subtypes are associated with the various pharmacological effects of the non-selective BZs. (hhs.gov)
Drugs2
- Reduced cerebral blood flow could be a factor in the uptake and penetration of lipophilic drugs such as MK-801 into brain tissue. (patentpc.com)
- The uptake of these drugs is severely affected by ischemia and reduced blood flow. (patentpc.com)
Brain1
- Proton Pump Inhibitors (PPIs) & Cognitive Impairment: Brain Not Working? (drewisdope.com)
Shows1
- This graph shows the total number of publications written about "GABA Agents" by people in this website by year, and whether "GABA Agents" was a major or minor topic of these publications. (musc.edu)
Increase1
- They also increase the frequency of chlorine channel opening in response to GABA binding. (medscape.com)