GABA receptors

The ionotropic y-aminobutiric acid receptors of GABAa type (Figure 5.5) are expressed by astroglial cells throughout the brain regions, including hippocampus, cerebellum, pituitary gland, optic nerve, retina and spinal cord, and in oligodendrocytes. Molecularly, these receptors are the same as neuronal ones, being in essence ligand-gated Cl- channels. Functionally, however, there is a remarkable difference, because glial cells contain much more Cl- than mature neurones (35 mM vs. ~3-5 mM) , and therefore the equilibrium potential for Cl- in astrocytes and oligodendrocytes is about -40 mV, whereas in neurones it lies somewhere near -70 mV. As a consequence, activation of GABAa receptors in glial cells triggers efflux of Cl- ions and cell depolarization. Interestingly, activation of GABAA receptors also inhibits astroglial K+ channels thus facilitating depolarization.

Figure 5.5 GABA receptors are represented by ionotropic GABAA/C receptors and metabotropic GABAB receptors. GABAA receptors are ligand gated Cl- channels, and on their activation Cl- moves according to the electrochemical gradient; in neurones, the equilibrium potential for Cl- (ECl) is -70 mV, and activation of GABAA receptors results in Cl- influx and hyperpolarization, whereas glia have a strongly negative resting membrane potential (Vm) and high intracellular Cl- concentration (ECl of -30 to -40 mV), so that activation of GABAA receptors results in Cl- efflux and depolarization. GABAB receptors are coupled to G proteins that control opening of K+ and Ca2+ channels

Figure 5.5 GABA receptors are represented by ionotropic GABAA/C receptors and metabotropic GABAB receptors. GABAA receptors are ligand gated Cl- channels, and on their activation Cl- moves according to the electrochemical gradient; in neurones, the equilibrium potential for Cl- (ECl) is -70 mV, and activation of GABAA receptors results in Cl- influx and hyperpolarization, whereas glia have a strongly negative resting membrane potential (Vm) and high intracellular Cl- concentration (ECl of -30 to -40 mV), so that activation of GABAA receptors results in Cl- efflux and depolarization. GABAB receptors are coupled to G proteins that control opening of K+ and Ca2+ channels

Some astroglial cells (e.g. in hippocampus) and OPCs express metabotropic GABAb receptors coupled with InsP3 metabolism and Ca2+ release from the intra-cellular stores.

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