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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Impaired motor coordination and Purkinje cell excitability in mice lacking calretinin.

In the cerebellum, the parallel fiber-Purkinje cell synapse can undergo long-term synaptic plasticity suggested to underlie motor learning and resulting from variations in intracellular calcium concentration ([Ca2+]i). Ca2+ binding proteins are enriched in the cerebellum, but their role in information processing is not clear. Here, we show that mice deficient in calretinin (Cr-/-) are impaired in tests of motor coordination. An impairment in Ca2+ homeostasis in Cr-/- Purkinje cells was supported by the high Ca2+-saturation of calbindin-D28k in these cells. The firing behavior of Purkinje cells is severely affected in Cr-/- alert mice, with alterations of simple spike firing rate, complex spike duration, and simple spike pause. In contrast, in slices, transmission at parallel fiber- or climbing fiber-Purkinje cell synapses is unaltered, indicating that marked modifications of the firing behavior in vivo can be undetectable in slice. Thus, these results show that calretinin plays a major role at the network level in cerebellar physiology.[1]

References

  1. Impaired motor coordination and Purkinje cell excitability in mice lacking calretinin. Schiffmann, S.N., Cheron, G., Lohof, A., d'Alcantara, P., Meyer, M., Parmentier, M., Schurmans, S. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
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