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 Ca 2+-spikes. The neurons normally discharge such spikes on low-threshold Ca 2+-spikes after the action potentials of a burst. We studied membrane mechanisms that regulate the discharge of high-threshold Ca 2+-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 Ca 2+-spike in the burst firing mode. Application of tetrodotoxin blocked the amplification and high-threshold Ca 2+-spike firing. A slowly inactivating K + conductance, sensitive to blockade with 4-aminopyridine (50–100 μM), but not tetraethylammonium (2–10 mM), appeared to suppress excitability and high-threshold Ca 2+-spike firing. Application of 4-aminopyridine increased the low-threshold Ca 2+-spike and the number of action potentials in the burst, and led to a conversion of the superimposed high-threshold Ca 2+-spike into a plateau potential. Application of the Ca 2+-channel blocker Cd 2+ (50 μM), 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 Ca 2+-spike firing, and a short-term influx of Ca 2+, are regulated by a balance of voltage-dependent conductances. Normally, a slowly inactivating A-type K +-conductance may reduce high-threshold Ca 2+-spike firing and shorten high-threshold Ca 2+-spike duration. A persistent Na +-conductance promotes coupling of the low-threshold Ca 2+-spike to a high-threshold Ca 2+-spike. Thus, the activation of both voltage-dependent conductances would affect Ca 2+ 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 states.