Editing GABA (section)

=== Neurotransmitter ===
Two general classes of [[GABA receptor]] are known:<ref>{{Cite book |last1=Marescaux |first1=C. |url=https://books.google.com/books?id=YggrBgAAQBAJ&pg=PT80 |title=Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors |last2=Vergnes |first2=M. |last3=Bernasconi |first3=R. |date=2013-03-08 |publisher=Springer Science & Business Media |isbn=978-3-7091-9206-1 |language=en}}</ref>
* [[GABAA receptor|GABA<sub>A</sub>]] in which the receptor is part of a [[ligand-gated ion channel]] complex<ref name="elifesciences.org">{{Cite journal |last1=Phulera |first1=Swastik |last2=Zhu |first2=Hongtao |last3=Yu |first3=Jie |last4=Claxton |first4=Derek P. |last5=Yoder |first5=Nate |last6=Yoshioka |first6=Craig |last7=Gouaux |first7=Eric |date=2018-07-25 |title=Cryo-EM structure of the benzodiazepine-sensitive α1β1γ2S tri-heteromeric GABA<sub>A</sub> receptor in complex with GABA |journal=eLife |language=en |volume=7 |pages=e39383 |doi=10.7554/eLife.39383 |doi-access=free |issn=2050-084X |pmc=6086659 |pmid=30044221}}</ref>
* [[GABAB receptor|GABA<sub>B</sub>]] [[metabotropic receptor]]s, which are [[G protein-coupled receptor]]s that open or close ion channels via intermediaries ([[G protein]]s)
[[File:Release, Reuptake, and Metabolism Cycle of GABA.png|class=skin-invert-image|alt=|thumb|500x500px|Release, reuptake, and metabolism cycle of GABA]]
Neurons that produce GABA as their output are called [[GABAergic]] neurons, and have chiefly inhibitory action at receptors in the adult vertebrate. [[Medium spiny neuron|Medium spiny cells]] are a typical example of inhibitory [[central nervous system]] GABAergic cells. In contrast, GABA exhibits both excitatory and inhibitory actions in [[insect]]s, mediating [[muscle]] activation at synapses between [[nerve]]s and muscle cells, and also the stimulation of certain [[gland]]s.<ref name="pmid8389005">{{cite journal |vauthors= Ffrench-Constant RH, Rocheleau TA, Steichen JC, Chalmers AE |title= A point mutation in a ''Drosophila'' GABA receptor confers insecticide resistance |journal= Nature |volume= 363 |issue= 6428 |pages= 449–51 |date= June 1993 |pmid= 8389005 |doi= 10.1038/363449a0 |bibcode= 1993Natur.363..449F|s2cid= 4334499 }}</ref> In mammals, some GABAergic neurons, such as [[chandelier cell]]s, are also able to excite their glutamatergic counterparts.<ref name="pmid16410524">{{cite journal |vauthors= Szabadics J, Varga C, Molnár G, Oláh S, Barzó P, Tamás G |title= Excitatory effect of GABAergic axo-axonic cells in cortical microcircuits |journal= Science |volume= 311 |issue= 5758 |pages= 233–235 |date= January 2006 |pmid= 16410524 |doi= 10.1126/science.1121325 |bibcode= 2006Sci...311..233S|s2cid= 40744562 }}</ref> In addition to fast-acting phasic inhibition, small amounts of extracellular GABA can induce slow timescale tonic inhibition on neurons.<ref name="Koh Kwak Cheong Lee 2023">{{cite journal |last1=Koh |first1=Wuhyun |last2=Kwak |first2=Hankyul |last3=Cheong |first3=Eunji |last4=Lee |first4=C. Justin |date=2023-07-26 |title=GABA tone regulation and its cognitive functions in the brain |journal=Nature Reviews Neuroscience |volume=24 |issue=9 |pages=523–539 |doi=10.1038/s41583-023-00724-7 |pmid=37495761 |s2cid=260201740 |issn=1471-003X}}</ref>   

[[GABAA receptor|GABA<sub>A</sub> receptors]] are ligand-activated chloride channels: when activated by GABA, they allow the flow of [[chloride]] ions across the membrane of the cell.<ref name="elifesciences.org"/> Whether this chloride flow is depolarizing (makes the voltage across the cell's membrane less negative), shunting (has no effect on the cell's membrane potential), or inhibitory/hyperpolarizing (makes the cell's membrane more negative) depends on the direction of the flow of chloride. When net chloride flows out of the cell, GABA is depolarising; when chloride flows into the cell, GABA is inhibitory or hyperpolarizing. When the net flow of chloride is close to zero, the action of GABA is shunting. [[Shunting inhibition]] has no direct effect on the membrane potential of the cell; however, it reduces the effect of any coincident synaptic input by reducing the [[electrical resistance and conductance|electrical resistance]] of the cell's membrane. 

Shunting inhibition can "override" the excitatory effect of depolarising GABA, resulting in overall inhibition even if the membrane potential becomes less negative. It was thought that a developmental switch in the molecular machinery controlling the concentration of chloride inside the cell changes the functional role of GABA between [[neonatal]] and adult stages. As the brain develops into adulthood, GABA's role changes from excitatory to inhibitory.<ref name="pmid18500393">{{cite journal |vauthors= Li K, Xu E |title= The role and the mechanism of γ-aminobutyric acid during central nervous system development |journal= Neurosci Bull |volume= 24 |issue= 3 |pages= 195–200 |date= June 2008 |pmid= 18500393 |pmc= 5552538 |doi= 10.1007/s12264-008-0109-3}}</ref>