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J Neurophysiol 82: 1218-1223, 1999;
0022-3077/99 $5.00
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The Journal of Neurophysiology Vol. 82 No. 3 September 1999, pp. 1218-1223
Copyright ©1999 by the American Physiological Society

GABAA-Dependent Chloride Influx Modulates GABAB-Mediated IPSPs in Hippocampal Pyramidal Cells

Valeri Lopantsev1 and Philip A. Schwartzkroin1,2

Departments of  1Neurological Surgery and  2Physiology and Biophysics, University of Washington, Seattle, Washington 98195-6470

Lopantsev, Valeri and Philip A. Schwartzkroin. GABAA-Dependent Chloride Influx Modulates GABAB-Mediated IPSPs in Hippocampal Pyramidal Cells. J. Neurophysiol. 82: 1218-1223, 1999. The relationship between postsynaptic inhibitory responses [the fast GABAA-mediated inhibitory postsynaptic potential (IPSP) and the slow GABAB-mediated IPSP] were investigated in hippocampal CA3 pyramidal cells. Mossy fiber-evoked GABAB-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, GABAB-mediated IPSPs were reduced at relatively depolarized levels (-55 mV) and enhanced at relatively hyperpolarized potentials (at least -60 mV). In contrast, the preceding GABAA-mediated IPSPs were larger at the more positive membrane potentials and smaller as the cell was hyperpolarized. Similar voltage dependency was obtained when monosynaptic GABAA- and GABAB-mediated IPSPs were isolated in the presence of glutamatergic receptor antagonists. However, monosynaptic GABAB-mediated IPSPs isolated in the presence of glutamatergic and GABAA receptor antagonists were not reduced at the more positive membrane potentials, and were significantly larger in amplitude than GABAB-mediated IPSPs preceded by a monosynaptic GABAA-mediated IPSP. The amplitude of the isolated monosynaptic GABAB-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 GABAA receptor-gated channels, modulates postsynaptic GABAB-mediated inhibition in hippocampal CA3 pyramidal cells.




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