Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 110, Issue 50, Pages 20302-20307Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1311686110
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Funding
- Centre National de la Recherche Scientifique (CNRS)
- Fondation pour la Recherche Medicale (FRM)/Universite Pierre et Marie Curie fellowship
- Region Ile de France
- CNRS
- Ecole Normale Superieure [ANR-08-SYSC-005, ANR-09-MNPS-38, ANR-11-BSV4-028, ANR-BLAN-SVSE4-LS-120230-DC/MM/, FRM DEQ20120323730]
- Dutch Organization for Medical Sciences
- Dutch Organization for Life Sciences
- Erasmus University Rotterdam Fellowship
- Center Neuro-Basic
- European Research Council Advanced grant
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Ca(V)3.1 T-type channels are abundant at the cerebellar synapse between parallel fibers and Purkinje cells where they contribute to synaptic depolarization. So far, no specific physiological function has been attributed to these channels neither as charge carriers nor more specifically as Ca2+ carriers. Here we analyze their incidence on synaptic plasticity, motor behavior, and cerebellar motor learning, comparing WT animals and mice where T-type channel function has been abolished either by gene deletion or by acute pharmacological blockade. At the cellular level, we show that Ca(V)3.1 channels are required for long-term potentiation at parallel fiber-Purkinje cell synapses. Moreover, basal simple spike discharge of the Purkinje cell in KO mice is modified. Acute or chronic T-type current blockade results in impaired motor performance in particular when a good body balance is required. Because motor behavior integrates reflexes and past memories of learned behavior, this suggests impaired learning. Indeed, subjecting the KO mice to a vestibulo-ocular reflex phase reversal test reveals impaired cerebellum-dependent motor learning. These data identify a role of low-voltage activated calcium channels in synaptic plasticity and establish a role for Ca(V)3.1 channels in cerebellar learning.
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