Cell-type-specific GABA responses and chloride homeostasis in the cortex and amygdala.
The GABA responses of fast-spiking (FS) interneurons and regular-spiking (RS) principal cells were studied using whole cell and perforated-patch recordings in slices of the basolateral amygdala, neo-, and perirhinal cortex. In these three areas, responses to exogenous and synaptically released GABA were abolished by GABA(A) receptor antagonists in FS cells but also included a GABA(B) component in RS cells. Moreover, E(GABA(A)) of FS and RS cells differed from the calculated E(Cl) (-61 mV), but in opposite direction (FS, -54 mV; RS, -72 mV). This was not due to a differential dialysis of FS and RS cells by the pipette solution because the discrepancy persisted when recordings were obtained with the perforated-patch-clamp technique, using the cation-selective ionophore gramicidin. Moreover, pharmacological inhibition of cation-chloride cotransporters revealed that the differing E(GABA(A)) of FS and RS neurons arises from cell-type-specific chloride homeostatic mechanisms. Indeed, the prevalent regulators of the intracellular chloride concentration are cotransporters that accumulate chloride in FS cells and extrude chloride in RS neurons. Thus, our results suggest that in the basolateral amygdala as well as in the parietal and perirhinal cortices, FS interneurons are more excitable than principal cells not only by virtue of their dissimilar electroresponsive properties but also because they express a different complement of GABA receptors and chloride homeostatic mechanisms.
Martina
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Laboratoire de Neurophysiologie, Département de Physiologie, Faculté de Médecine, Université Laval, Québec, Quebec G1K 7P4, Canada.
Royer
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Paré
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D000679:Amygdala / Q000378:metabolism*; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D002540:Cerebral Cortex / Q000378:metabolism*; D002712:Chlorides / Q000378:metabolism*; D004232:Diuretics / Q000494:pharmacology; D004558:Electric Stimulation; D058785:GABA-A Receptor Agonists; D058787:GABA-A Receptor Antagonists; D058786:GABA-B Receptor Agonists; D058788:GABA-B Receptor Antagonists; D006096:Gramicidin / Q000494:pharmacology; D006168:Guinea Pigs; D006706:Homeostasis / Q000502:physiology*; D066298:In Vitro Techniques; D007395:Interneurons / Q000502:physiology; D008564:Membrane Potentials / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D018408:Patch-Clamp Techniques; D011963:Receptors, GABA-A / Q000502:physiology; D018080:Receptors, GABA-B / Q000502:physiology; D012964:Sodium / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism / Q000502:physiology*
D000900:Anti-Bacterial Agents; D002712:Chlorides; D004232:Diuretics; D058785:GABA-A Receptor Agonists; D058787:GABA-A Receptor Antagonists; D058786:GABA-B Receptor Agonists; D058788:GABA-B Receptor Antagonists; D011963:Receptors, GABA-A; D018080:Receptors, GABA-B; D006096:Gramicidin; D013779:Tetrodotoxin; D005680:gamma-Aminobutyric Acid; D012964:Sodium