SYNAPTIC AND SYNAPTICALLY-ACTIVATED INTRINSIC CONDUCTANCES UNDERLIE INHIBITORY POTENTIALS IN CAT LATERAL AMYGDALOID PROJECTION NEURONS IN VIVO . Lang, E. J. and D. Par[acute]e. D[acute]epartement de Physiologie, Universit[acute]e Laval, Qu[acute]ebec, QU[acute]e. Canada G1K 7P4.
APStracts 3:0237N, 1996.
ABSTRACT
The companion paper (Lang and Par[acute]e 1996) demonstrated that the synaptic responsiveness of lateral amygdaloid (LAT) projection neurons is dominated by large, monophasic hyperpolarizing potentials. To characterize these responses, intracellular recordings were obtained from identified LAT projection neurons in barbiturate anesthetized cats. The reversal potential of cortically-evoked responses was measured at their peak, and 115 msec later (tail), an interval corresponding to the peak latency of the GABA B response previously recorded in vitro . With K-acetate (KAc) pipettes, these reversal potentials were -86.9 +/- 1.6 mV (peak; mean +/- SE) and -90.7 +/- 1.7 mV (tail), suggesting that Cl - and K + conductances contribute throughout the response. The small difference between the two reversals suggested an additional slowly activating K + -mediated component was present. To determine if Cl - conductances contributed to the response, recordings were performed with KCl. The peak (- 57.8 +/- 2.2 mV) and tail (-61.3 +/- 2.1 mV) reversals were 15-20 mV more positive than KAc values. The difference between the peak and tail reversals remained. Recordings were then obtained with pipettes filled with KAc or KCl and 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS), a Cl - pump blocker that has been reported to block GABA A responses. With KAc and DIDS, the initial depolarization was prolonged and the hyperpolarization amplitude decreased relative to that with KAc alone. However, with KCl and DIDS, the reversal was shifted even further, and the response consisting entirely of a large depolarization that produced a spike burst. Thus LAT neurons appear to have a DIDS-sensitive Cl - pump, but DIDS-resistant Cl - channels. To assess the contribution of K + conductances to the responses, recordings were obtained with CsAc pipettes. CsAc shifted the response reversal positively (peak, -71.9 +/- 1.0 mV; tail, -72.0 +/- 0.9 mV) compared to KAc values, and eliminated the difference between peak and tail reversals. Further, spikes generated under Cs + had a broad shoulder, presumably resulting from activation of dendritic Ca 2+ conductances. Spontaneous and evoked IPSPs dramatically reduced this shoulder suggesting that activation of dendritic conductances by back-propagating spikes is regulated by synaptic events. Intracellular injection of the Ca 2+ chelator caused a depolarization of the peak (-75.3 +/- 1.3 mV) and tail (-77.7 +/- 1.7 mV) reversals over 15-45 minutes. Concurrently, the EPSP amplitude increased and the hyperpolarization amplitude decreased, suggesting that Ca 2+ -dependent K + conductances contribute to the response. In conclusion, the large hyperpolarizing potentials regulating the excitability of LAT projection neurons appear to be mediated primarily by a Cl - , presumably GABA A , IPSP, and a synaptically- activated Ca 2+ -dependent K + conductance. A relatively weak K + -mediated, possibly GABA B , IPSP may contribute to the later portions of the response.

Received 7 May 1996; accepted in final form 27 September 1996.
APS Manuscript Number J375-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996