title: GABAA-responses of CA3 neurones: contribution of bicarbonate and of Cl(-)-extrusion mechanisms.
abstract: Postsynaptic GABAA-responses of cortical neurones may be composed of an early 'somatic' hyperpolarization (h-GABAA) and a 'dendritic' depolarization (d-GABAA). In order to study underlying anion-fluxes the gradient of bicarbonate across the membrane of CA3-neurones in hippocampal slices (guinea-pig) was reduced by several manoeuvres (NH4-prepulse-technique, CO2/bicarbonate-withdrawal-technique, acetazolamide, DIDS). Each manoeuvre resulted in an attenuation of d-GABAA. The inhibition of a Cl-/bicarbonate-exchanger with DIDS could also weaken h-GABAA which was selectively impaired by ethacrynic acid--known to block an ATP-driven somatic Cl(-)-extrusion mechanism. In conclusion, bicarbonate-fluxes contribute to d-GABAA rather than to h-GABAA which is mainly driven by Cl(-)-fluxes. An uneven distribution of Cl(-)-extrusion mechanisms along the adult CA3-neurones is likely to build up the anion-gradients necessary to generate biphasic GABAA-responses.
authors.affiliation: Institut für Physiologie, Universität-GH Essen, Germany.
authors.forename: U
authors.initials: U
authors.lastname: Bonnet
authors.forename: D
authors.initials: D
authors.lastname: Bingmann
mesh_terms: D000086:Acetazolamide / Q000494:pharmacology; D000818:Animals; D017920:Antiporters / Q000378:metabolism*; D001639:Bicarbonates / Q000378:metabolism*; D027963:Chloride-Bicarbonate Antiporters; D002712:Chlorides / Q000378:metabolism*; D004976:Ethacrynic Acid / Q000494:pharmacology; D006168:Guinea Pigs; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects*; D066298:In Vitro Techniques; D009474:Neurons / Q000187:drug effects*; D011963:Receptors, GABA-A / Q000502:physiology*
chemical_list: D017920:Antiporters; D001639:Bicarbonates; D027963:Chloride-Bicarbonate Antiporters; D002712:Chlorides; D011963:Receptors, GABA-A; D004976:Ethacrynic Acid; D000086:Acetazolamide