Modulation of bursts and high-threshold calcium spikes in neurons of rat auditory thalamus

Neurons in the ventral partition of the medial geniculate body are able to fire high-threshold Ca2+-spikes. The neurons normally discharge such spikes on low-threshold Ca2+-spikes after the action potentials of a burst. We studied membrane mechanisms that regulate the discharge of high-threshold Ca2+-spikes, using whole-cell recording techniques in a slice preparation of rat thalamus. A subthreshold (persistent) Na+-conductance amplified depolarizing inputs, enhancing membrane excitability in the tonic firing mode and amplifying the low-threshold Ca2+-spike in the burst firing mode. Application of tetrodotoxin blocked the amplification and high-threshold Ca2+-spike firing. A slowly inactivating K+ conductance, sensitive to blockade with 4-aminopyridine (50-100 mu M), but not tetraethylammonium (2-10 mM), appeared to suppress excitability and high-threshold Ca2+-spike firing. Application of 4-aminopyridine increased the low-threshold Ca2+-spike and the number of action potentials in the burst, and led to a conversion of the superimposed high-threshold Ca2+-spike into a plateau potential. Application of the Ca2+-channel blocker Cd2+ (50 mu M), reduced or eliminated this plateau potential. The tetrodotoxin sensitive, persistent Na+-conductance also sustained plateau potentials, triggered after 4-aminopyridine application on depolarization by current pulses. Our results suggest that high-threshold Ca2+-spike firing, and a short-term influx of Ca2+, are regulated by a balance of voltage-dependent conductances. Normally, a slowly inactivating A-type K+-conductance may reduce high-threshold Ca2+-spike firing and shorten high-threshold Ca2+-spike duration. A persistent Na+-conductance promotes coupling of the low-threshold Ca2+-spike to a high-threshold Ca2+-spike. Thus, the activation of both voltage-dependent conductances would affect Ca2+ influx into ventral medial geniculate neurons. This would alter the quality of the different signals transmitted in the thalamocortical system during wakefulness, sleep and pathological stares. (C) 1998 IBRO. Published by Elsevier Science Ltd.