When net chloride flows out of the cell, GABA is depolarising; when chloride flows into the cell, GABA is inhibitory or hyperpolarizing.
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When net chloride flows out of the cell, GABA is depolarising; when chloride flows into the cell, GABA is inhibitory or hyperpolarizing.
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Shunting inhibition can "override" the excitatory effect of depolarising GABA, resulting in overall inhibition even if the membrane potential becomes less negative.
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GABA is an inhibitory transmitter in the mature brain; its actions were thought to be primarily excitatory in the developing brain.
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Besides the nervous system, GABA is produced at relatively high levels in the insulin-producing ß-cells of the pancreas.
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In 2018, GABA has shown to regulate secretion of a greater number of cytokines.
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The conformational flexibility of GABA is important for its biological function, as it has been found to bind to different receptors with different conformations.
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In 1883, GABA was first synthesized, and it was first known only as a plant and microbe metabolic product.
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In 1950, GABA was discovered as an integral part of the mammalian central nervous system.
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GABA is primarily synthesized from glutamate via the enzyme glutamate decarboxylase with pyridoxal phosphate as a cofactor.
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GABA can be synthesized from putrescine by diamine oxidase and aldehyde dehydrogenase.
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Traditionally it was thought that exogenous GABA did not penetrate the blood–brain barrier, however more current research describes the notion as being unclear pending further research.
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GABA directly injected to the brain has been reported to have both stimulatory and inhibitory effects on the production of growth hormone, depending on the physiology of the individual.
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GABA is not an alpha amino acid, meaning the amino group is not attached to the alpha carbon.
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