[Regulation of GABA receptors by intracellular factors].
gamma-Aminobutyric acid (GABA) directly inhibits the postsynaptic membrane through GABAA receptor Cl- channel complexes. This inhibition is promoted or blocked by various intra- and extracellular substances at the site of either receptor or channel. Recent studies focused on the intracellular inhibitory mechanisms of the GABAergic response in neurons: one is the inhibition of GABA receptors by the increase in intracellular Ca2+ and the other is inhibition through ATP receptors triggered by the decrease in intracellular ATP level. In addition, the spontaneous inhibitory postsynaptic currents (IPSCs) induced by GABA released from the nerve terminals were suppressed by activation of the GABAB receptor, which acts as a negative autoreceptor in the nerve ending. The intracellular mechanism of the suppression will be discussed.
Akaike
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Department of Neurophysiology, Tohoku University School of Medicine, Sendai, Japan.
D000255:Adenosine Triphosphate / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000502:physiology; D006801:Humans; D011963:Receptors, GABA-A / Q000502:physiology*
D011963:Receptors, GABA-A; D000255:Adenosine Triphosphate; D002118:Calcium