Ionic Factors Governing Rebound Burst Phenotype in Rat Deep Cerebellar Neurons

Abstract

Large diameter cells in rat deep cerebellar nuclei (DCN) can be distinguished according to the generation of a transient or weak rebound burst and the expression of T-type Ca2+ channel isoforms. We studied the ionic basis for the distinction in burst phenotypes in rat DCN cells in vitro. Following a hyperpolarization, transient burst cells generated a high-frequency spike burst of ≤450 Hz, whereas weak burst cells generated a lower-frequency increase (<140 Hz). Both cell types expressed a low voltage–activated (LVA) Ca2+ current near threshold for rebound burst discharge (−50 mV) that was consistent with T-type Ca2+ current, but on average 7 times more current was recorded in transient burst cells. The number and frequency of spikes in rebound bursts was tightly correlated with the peak Ca2+ current at −50 mV, showing a direct relationship between the availability of LVA Ca2+ current and spike output. Transient burst cells exhibited a larger spike depolarizing afterpotential that was insensitive to blockers of voltage-gated Na+ or Ca2+ channels. In comparison, weak burst cells exhibited larger afterhyperpolarizations (AHPs) that reduced cell excitability and rebound spike output. The sensitivity of AHPs to Ca2+ channel blockers suggests that both LVA and high voltage–activated (HVA) Ca2+ channels trigger AHPs in weak burst compared with only HVA Ca2+ channels in transient burst cells. The two burst phenotypes in rat DCN cells thus derive in part from a difference in the availability of LVA Ca2+ current following a hyperpolarization and a differential activation of AHPs that establish distinct levels of membrane excitability.