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Altered Purkinje cell responses and calmodulin expression in the spontaneously ataxic mouse, Pogo
Author(s) -
Lee Kwan Young,
Kim Jin Seong,
Kim Se Hoon,
Park Hyung Seo,
Jeong YoungGil,
Lee NamSeob,
Kim Dong Kwan
Publication year - 2011
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.1460-9568.2011.07641.x
Subject(s) - calmodulin , climbing fiber , cerebellum , neuroscience , excitatory postsynaptic potential , purkinje cell , ataxia , chemistry , antagonist , parallel fiber , patch clamp , biology , electrophysiology , calcium , receptor , inhibitory postsynaptic potential , biochemistry , organic chemistry
Ataxia is often associated with altered cerebellar motor control, a process in which Purkinje cells (PCs) play a principal role. Pogo mice display severe motor deficits characterized by an ataxic gait accompanying hindlimb hyperextension. Here, using whole‐cell patch‐clamp recordings, we show that parallel fiber (PF)‐excitatory post‐synaptic currents (PF‐EPSCs) are reduced, paired‐pulse facilitation (PPF) is increased and PF‐PC long‐term depression (LTD) is impaired in Pogo mice; in contrast, climbing‐fiber EPSCs are preserved. In control mice, treatment with the calmodulin antagonist calmidazolium (5 μ m ) impaired PPF and LTD. Notably, cerebellar calmodulin expression was significantly reduced in Pogo mice compared with control mice. Control PCs predominantly exhibited a tonic firing pattern, whereas the firing pattern in Pogo PCs was mainly a complex burst type. These results implicate alterations in PC responses and calmodulin content in the abnormal cerebellar function of Pogo mice.