GABAA-Receptor-Mediated Rebound Burst Firing and Burst Shunting in Thalamus

Publisher Website
Google Scholar
Abstract
Ulrich, Daniel and John R. Huguenard. GABAA-receptor-mediated rebound burst firing and burst shunting in thalamus. J. Neurophysiol. 78: 1748–1751, 1997. The role of γ-aminobutyricacid-A (GABAA)-receptor-mediated inhibitory postsynaptic potentials (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 six or more 10-nS GABAA IPSPs generated rebound bursts of action potentials with a mean delay of 605 ± 32 (SE) ms. In contrast, 10 IPSPs were required for rebound bursts in relay cells, and these occurred with a significantly shorter delay of 327 ± 35 ms. 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 (∼20 ms) than TC cells (∼10 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.