GABAA receptor-mediated rebound burst firing and burst shunting in
thalamus.
Daniel Ulrich and John R. Huguenard.
Stanford University School of Medicine. Stanford CA 94305. U.S.A.
APStracts 4:01027N, 1997.
ABSTRACT
The role of GABAA-receptor mediated IPSPs in 1) generating rebound burst-
firing and 2) burst-inhibition in thalamocortical (TC) relay cells and
inhibitory neurons of nucleus reticularis thalami (nRt) was investigated.
Experimental data from previous studies were used to generate artificial
synaptic responses in neurons via a computer-driven dynamic clamp. On average,
in nRt neurons trains of 6 or more 10 nS GABAA IPSPs generated rebound-bursts
of action potentials with a mean delay of 605 ñ 32 ms. In contrast, 10 IPSPs
were required for rebound bursts in relay cells, and these occurred with a
significantly shorter delay of 327 ñ 35ms. Ca2+-dependent burst responses
could be shunted by single IPSPs. Half-maximal burst inhibition was obtained
in nRt cells when IPSP conductance was 1.5 times the whole-cell input
conductance. Burst shunting in TC cells was less effective, and required a
synaptic to input conductance ratio of 3. The relative time window of IPSP
burst-shunting was broader in nRt (ÿ7E20 ms) than TC cells (ÿ7E10 ms).
We conclude that in nRt cells GABAA-dependent rebound burst responses would
occur with a latency that is incompatible with pacemaking of fast (>3 Hz)
thalamic rhythm generation such as spindles, yet burst inhibition is powerful.
Therefore, a likely role for reciprocal intra-nRt connectivity is to mediate
lateral inhibition between nRt cells.
Received 31 March 1997; accepted in final form 14 May 1997.
APS Manuscript Number J178-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 15 July 1997