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This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 561/3/703    most recent jphysiol.2004.071696v1 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zhang, W. Articles by Linden, D. J Search for Related Content PubMed PubMed Citation Articles by Zhang, W. Articles by Linden, D. J

¹ Department of Neuroscience, The Johns Hopkins University School of Medicine, 725 N. Wolfe Street, 916 Hunterian Building, Baltimore, MD 21205, USA

The deep cerebellar nuclei (DCN) are the major output of the cerebellum, and have been proposed as a site of memory storage for certain forms of motor learning. Microelectrode and whole-cell patch recordings were performed on DCN neurones in acute slices of juvenile rat cerebellum. DCN neurones display tonic and bursting basal firing patterns. In tonically firing neurones, a stimulus consisting of EPSP bursts produced a brief increase in dendritic Ca²⁺ concentration and a persistent increase in the number of spikes elicited by a depolarizing test pulse, along with a decrease in spike threshold. In intrinsically bursting DCN neurones, EPSP bursts induced an increase in the number of depolarization-evoked spikes in some neurones, but in others produced a change to a more tonic firing pattern. Application of IPSP bursts evoked a large number of rebound spikes and an associated dendritic Ca²⁺ transient, which also produced a persistent increase in the number of spikes elicited by a test pulse. Intracellular perfusion of the Ca²⁺ chelator BAPTA prevented the increase in intrinsic excitability. Thus, rapid changes in intrinsic excitability in the DCN may be driven by bursts of both EPSPs and IPSPs, and may result in persistent changes to both firing frequency and pattern.

(Received 12 July 2004; accepted after revision 18 October 2004; first published online 21 October 2004)
Corresponding author D. J. Linden: Department of Neuroscience, The Johns Hopkins University School of Medicine, 725 N. Wolfe Street, 916 Hunterian Building, Baltimore, MD 21205, USA. Email: dlinden{at}jhmi.edu

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