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This Article Full Text Full Text (PDF) All Versions of this Article: 100/5/2684    most recent 90427.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Molineux, M. L. Articles by Turner, R. W. PubMed PubMed Citation Articles by Molineux, M. L. Articles by Turner, R. W.

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.