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GABA: Difference between revisions
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{{DepressantOD| | {{DepressantOD|GABAergics}} | ||
[[File:GABA. | [[File:GABA.svg|250px|thumb|right|Skeletal structure of the GABA molecule.]] | ||
'''GABA''', also known as '''gamma-aminobutyric acid''', is the main inhibitory neurotransmitter. Drugs targeting GABA include [[Benzodiazepine|benzodiazepines]], [[barbiturates]], [[alcohol]] and [[GHB]]. | '''GABA''', also known as '''gamma-aminobutyric acid''', is the main inhibitory [[neurotransmitter]]. Drugs targeting GABA include [[Benzodiazepine|benzodiazepines]], [[barbiturates]], [[alcohol]] and [[GHB]]/[[GBL]]. | ||
A | A GABAergic agent is a substance which functions to directly modulate the GABA system, the main inhibitory neurotransmitter, in the body or brain. This can include GABA [[receptor]] [[agonist]]s, GABA receptor antagonists, and GABA [[reuptake inhibitor]]s. | ||
Substances that indirectly modulate the GABA system are known as "positive allosteric modulators", and includes [[barbiturates]] and [[benzodiazepines]] as well as [[alcohol]]. [[Flumazenil]] is an example of a "negative allosteric modulator".{{citation needed}} | |||
==Chemistry== | ==Chemistry== | ||
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GABA is synthesized from [[glutamate]] via the enzyme glutamic acid decarboxylase (GAD). When GABA is released into the [[synapse]], it binds to and activates GABA receptors. This activation is terminated by reuptake back up into the cell that released it and into nearby glial cells. GABA that is taken back into the neuron can be used; however, GABA that enters [[glia]], the supporting cells that surround [[neurons]], cannot be re-synthesized as glial cells lack GAD. | GABA is synthesized from [[glutamate]] via the enzyme glutamic acid decarboxylase (GAD). When GABA is released into the [[synapse]], it binds to and activates GABA receptors. This activation is terminated by reuptake back up into the cell that released it and into nearby glial cells. GABA that is taken back into the neuron can be used; however, GABA that enters [[glia]], the supporting cells that surround [[neurons]], cannot be re-synthesized as glial cells lack GAD. | ||
GABA is metabolized by the enzyme GABA transaminase and certain drugs (such as the antiepileptic [[vigabatrin]]) have inhibition of this enzyme as their mechanism of action. Eventually, GABA can be recovered by its metabolite succinic semialdehyde which is transformed by succinic semialdehyde dehydrogenase into succinic acid and enters the Krebs cycle, a complicated pathway that begins with glucose. On the other end of the cycle, glutamine emerges and can be transported back to the neuron where it is converted by the enzyme glutaminase into glutamate which can then be remade into GABA via GAD, completing the loop. This loop is called the GABA shunt.<ref>GABA Synthesis, Uptake and Release | GABA is metabolized by the enzyme GABA transaminase and certain drugs (such as the antiepileptic [[vigabatrin]]) have inhibition of this enzyme as their mechanism of action. Eventually, GABA can be recovered by its metabolite succinic semialdehyde which is transformed by succinic semialdehyde dehydrogenase into succinic acid and enters the Krebs cycle, a complicated pathway that begins with glucose. On the other end of the cycle, glutamine emerges and can be transported back to the neuron where it is converted by the enzyme glutaminase into glutamate which can then be remade into GABA via GAD, completing the loop. This loop is called the GABA shunt.<ref>{{cite journal | vauthors=((Olsen, R. W.)), ((DeLorey, T. M.)) | journal=Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition | title=GABA Synthesis, Uptake and Release | date= 1999 | url=https://www.ncbi.nlm.nih.gov/books/NBK27979/}}</ref> | ||
== Pharmacology == | |||
Drugs that act as allosteric modulators of GABA receptors (known as GABA analogues or ''GABAergic'' drugs), or increase the available amount of GABA, typically have relaxing, anti-anxiety, and anti-convulsive effects.<ref>{{cite journal | vauthors=((Foster, A.)), ((Kemp, J.)) | journal=Current Opinion in Pharmacology | title=Glutamate- and GABA-based CNS therapeutics | volume=6 | issue=1 | pages=7–17 | date= February 2006 | url=https://linkinghub.elsevier.com/retrieve/pii/S1471489205001918 | issn=14714892 | doi=10.1016/j.coph.2005.11.005}}</ref> | |||
In general, GABA does not cross the blood–brain barrier,<ref>{{cite journal | vauthors=((Kuriyama, K.)), ((Sze, P. Y.)) | journal=Neuropharmacology | title=Blood-brain barrier to H3-γ-aminobutyric acid in normal and amino oxyacetic acid-treated animals | volume=10 | issue=1 | pages=103–108 | date= January 1971 | url=https://linkinghub.elsevier.com/retrieve/pii/002839087190013X | issn=00283908 | doi=10.1016/0028-3908(71)90013-X}}</ref> although certain areas of the brain that have no effective blood–brain barrier, such as the periventricular nucleus, can be reached by drugs such as systemically injected GABA.<ref>{{cite journal | vauthors=((Müller, E. E.)), ((Locatelli, V.)), ((Cocchi, D.)) | journal=Physiological Reviews | title=Neuroendocrine control of growth hormone secretion | volume=79 | issue=2 | pages=511–607 | date= April 1999 | issn=0031-9333 | doi=10.1152/physrev.1999.79.2.511}}</ref> | |||
==Inhibitory response== | ==Inhibitory response== | ||
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===Drugs targeting [[GABA-A|GABA<sub>A</sub>]]=== | ===Drugs targeting [[GABA-A|GABA<sub>A</sub>]]=== | ||
====[[Benzodiazepine|Benzodiazepines]]==== | ====[[Benzodiazepine|Benzodiazepines]]==== | ||
* [[Alprazolam]] | |||
* [[Clonazepam]] | *[[Alprazolam]] | ||
* [[Clonazolam]] | *[[Clonazepam]] | ||
* [[Diazepam]] | *[[Clonazolam]] | ||
* [[Diclazepam]] | *[[Diazepam]] | ||
* [[Flubromazolam]] | *[[Diclazepam]] | ||
* [[Flubromazepam]] | *[[Flubromazolam]] | ||
* [[Nifoxipam]] | *[[Flubromazepam]] | ||
* [[Lorazepam]] | *[[Nifoxipam]] | ||
* [[Phenazepam]] | *[[Lorazepam]] | ||
* [[Pyrazolam]] | *[[Phenazepam]] | ||
* [[Temazepam]] | *[[Pyrazolam]] | ||
*[[Temazepam]] | |||
*[[Triazolam]] | |||
====[[Thienodiazepine|Thienodiazepines]]==== | ====[[Thienodiazepine|Thienodiazepines]]==== | ||
* [[Etizolam]] | |||
* [[Deschloroetizolam]] | *[[Etizolam]] | ||
* [[Metizolam]] | *[[Deschloroetizolam]] | ||
*[[Metizolam]] | |||
====Others==== | ====Others==== | ||
* [[ | |||
* [[ | *[[Alcohol]] | ||
* [[ | *[[2-Methyl-2-butanol]] | ||
* [[ | *[[Barbiturates]] | ||
* [[Methaqualone]] | *[[Carisoprodol]] | ||
* [[ | *[[Isopropanol]]{{citation needed}} | ||
* [[ | *[[Methaqualone]] | ||
* [[ | *[[Methanol]]{{citation needed}} | ||
* [[ | *[[Amanita muscaria|Muscimol]] | ||
*[[Zaleplon]] | |||
*[[Zopiclone]] | |||
*[[Zolpidem]] | |||
===Drugs targeting [[GABA-B|GABA<sub>B</sub>]]=== | ===Drugs targeting [[GABA-B|GABA<sub>B</sub>]]=== | ||
Drugs targeting [[GABA-B|GABA<sub>B</sub>]] are more scarce, chiefly consisting of [[phenibut]], [[baclofen]], [[GHB]], [[1,4-Butanediol]], | Drugs targeting [[GABA-B|GABA<sub>B</sub>]] are more scarce, chiefly consisting of [[phenibut]], [[F-phenibut]], [[baclofen]], [[GHB]], [[1,4-Butanediol]], and [[GBL]]. | ||
==GABAergic dependence and withdrawal== | ==GABAergic dependence and withdrawal== | ||
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==See also== | ==See also== | ||
*[[Responsible use]] | *[[Responsible use]] | ||
*[[Acetylcholine]] | *[[Acetylcholine]] | ||
*[[Glutamate]] | *[[Glutamate]] | ||
*[[ | *[[Pregabalin]] | ||
*[[ | *[[Gabapentin]] | ||
*[[ | |||
==External links== | |||
*[[wikipedia:gamma-Aminobutyric acid|''gamma''-Aminobutyric acid (Wikipedia)]] | |||
==References== | ==References== | ||
<references/> | <references /> | ||
[[Category:Neurotransmitter]] | |||
[[Category:Gamma-Amino acid]] | |||
{{#set:Featured=true}} | |||