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Ionic Factors Governing Rebound Burst Phenotype in Rat Deep Cerebellar Neurons

Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada

Submitted 1 April 2008; accepted in final form 27 August 2008

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.

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