title: GABAA-Dependent chloride influx modulates GABAB-mediated IPSPs in hippocampal pyramidal cells.
abstract: The relationship between postsynaptic inhibitory responses [the fast GABA(A)-mediated inhibitory postsynaptic potential (IPSP) and the slow GABA(B)-mediated IPSP] were investigated in hippocampal CA3 pyramidal cells. Mossy fiber-evoked GABA(B)-mediated IPSPs were, paradoxically, of greater amplitude in cells with resting membrane potential of -62 mV (13.6 +/- 0.5 mV; mean +/- SE) as compared with cells with resting membrane potential of -54 mV (7.0 +/- 0.8 mV). In addition, when a cell's membrane potential was artificially manipulated, GABA(B)-mediated IPSPs were reduced at relatively depolarized levels (-55 mV) and enhanced at relatively hyperpolarized potentials (at least -60 mV). In contrast, the preceding GABA(A)-mediated IPSPs were larger at the more positive membrane potentials and smaller as the cell was hyperpolarized. Similar voltage dependency was obtained when monosynaptic GABA(A)- and GABA(B)-mediated IPSPs were isolated in the presence of glutamatergic receptor antagonists. However, monosynaptic GABA(B)-mediated IPSPs isolated in the presence of glutamatergic and GABA(A) receptor antagonists were not reduced at the more positive membrane potentials, and were significantly larger in amplitude than GABA(B)-mediated IPSPs preceded by a monosynaptic GABA(A)-mediated IPSP. The amplitude of the isolated monosynaptic GABA(B)-mediated IPSPs recorded with potassium chloride-containing microelectrodes was significantly smaller than the comparable potential recorded with potassium acetate microelectrodes without chloride. We conclude that voltage-dependent chloride influx, via GABA(A) receptor-gated channels, modulates postsynaptic GABA(B)-mediated inhibition in hippocampal CA3 pyramidal cells.
authors.affiliation: Department of Neurological Surgery, University of Washington, Seattle, Washington 98195-6470, USA.
authors.forename: V
authors.initials: V
authors.lastname: Lopantsev
authors.forename: P A
authors.initials: PA
authors.lastname: Schwartzkroin
mesh_terms: D000818:Animals; D004594:Electrophysiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D006624:Hippocampus / Q000166:cytology / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology*; D017966:Pyramidal Cells / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011963:Receptors, GABA-A / Q000502:physiology*; D018080:Receptors, GABA-B / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*
chemical_list: D018691:Excitatory Amino Acid Antagonists; D058787:GABA-A Receptor Antagonists; D011963:Receptors, GABA-A; D018080:Receptors, GABA-B