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Mono‐ and dual‐frequency fast cerebellar oscillation in mice lacking parvalbumin and/or calbindin D‐28k
Author(s) -
Servais L.,
Bearzatto B.,
Schwaller B.,
Dumont M.,
De Saedeleer C.,
Dan B.,
Barski J. J.,
Schiffmann S. N.,
Cheron G.
Publication year - 2005
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2005.04275.x
Subject(s) - parvalbumin , calbindin , purkinje cell , neuroscience , oscillation (cell signaling) , cerebellar cortex , inhibitory postsynaptic potential , rhythm , biology , cerebellum , chemistry , biophysics , medicine , endocrinology , calcium , biochemistry
Calbindin is a fast Ca 2+ ‐binding protein expressed by Purkinje cells and involved in their firing regulation. Its deletion produced ∼160‐Hz oscillation sustained by synchronous, rhythmic Purkinje cells in the cerebellar cortex of mice. Parvalbumin is a slow‐onset Ca 2+ ‐binding protein expressed in Purkinje cells and interneurons. In order to assess its function in Purkinje cell firing regulation, we studied the firing behavior of Purkinje cells in alert mice lacking parvalbumin (PV –/– ), calbindin (CB –/– ) or both (PV –/– CB –/– ) and in wild‐type controls. The absence of either protein resulted in Purkinje cell firing alterations (decreased complex spike duration and pause, increased simple spike firing rate) that were more pronounced in CB –/– than in PV –/– mice. Cumulative effects were found in complex spike alterations in PV –/– CB –/– mice. PV –/– and CB –/– mice manifested ∼160‐Hz oscillation that was sustained by Purkinje cells firing rhythmically and synchronously along the parallel fiber axis. This oscillation was dependent on GABA A , N ‐methyl‐ d ‐aspartate and gap junction transmission. PV –/– CB –/– mice exhibited a dual‐frequency (110 and 240 Hz) oscillation. The instantaneous spectral densities of both components were inversely correlated. Simple and complex spikes of Purkinje cells were phase‐locked to one of the two oscillation frequencies. Mono‐ and dual‐frequency oscillations presented similar pharmacological properties. These results demonstrate that the absence of the Ca 2+ buffers parvalbumin and calbindin disrupts the regulation of Purkinje cell firing rate and rhythmicity in vivo and suggest that precise Ca 2+ transient control is required to maintain the normal spontaneous arrhythmic and asynchronous firing pattern of the Purkinje cells.