Hyperpolarization-induced rebound spiking has been identified as an important mechanism that may be involved in the control of deep cerebellar nucleus (DCN) spiking by Purkinje cell input. The IH current has previously been identified to contribute to the rebound depolarization (RD) underlying rebound spiking in DCN neurons, but a detailed study of all conductances involved has not been performed. In the present study we examine the voltage-gated conductances underlying multiple components of the rebound. Using whole cell recordings in rat brain slices, we studied current clamp records of rebound spiking induced by negative current injections of varying duration. We find that up to three components of rebound spiking can be identified. A very short high-frequency rebound burst was present only in subpopulation of cells. This fast burst survived IH block with 5 mM cesium and a brief RD was revealed with TTX block of Na currents, suggesting that the underlying conductance is a T-type calcium current. A rebound lasting up to several seconds was observed in most cells. IH block with 5 mM Cs did not abolish this long lasting rebound, but delayed its onset, indicating that IH is responsible for the rapid onset of the prolonged rebound but does not control its late phase. Furthermore, IH block generally promoted bistability of DCN firing and increased firing frequencies during slow rebounds. Application of Cd, Ni, and Nifedpine did not remove the slow RD response and spike frequency increase, indicating that Ca currents were not responsible for inducing long lasting rebounds. TTX eliminated any long lasting RD, suggesting that it is caused by a persistent Na current. Currents mimicking a persistent Na current were simulated in real time using a Hodgkin-Huxley formalism, and were applied via dynamic clamping. Addition of the simulated current enhanced long-lasting rebound spiking, while subtraction abolished slow rebound spiking.
Support Contributed By: NINH grant R01-MH065634
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