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.
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