Source:http://linkedlifedata.com/resource/pubmed/id/21621520
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
|
pubmed:dateCreated |
2011-6-27
|
pubmed:abstractText |
T-type Ca(2+) channels have been implicated in tremorogenesis and motor coordination. The ?1 subunit of the Ca(V)3.1 T-type Ca(2+) channel is highly expressed in motor pathways in the brain, but knockout of the Ca(V)3.1 gene (?(1G)(-/-)) per se causes no motor defects in mice. Thus, the role of Ca(V)3.1 channels in motor control remains obscure in vivo. Here, we investigated the effect of the Ca(V)3.1 knockout in the null genetic background of ?1 GABA(A) receptor (?1(-/-)) by generating the double mutants (?1(-/-)/?(1G)(-/-)). ?1(-/-)/?(1G)(-/-) mice showed severer motor abnormalities than ?1(-/-) mice as measured by potentiated tremor activities at 20Hz and impaired motor learning. Propranolol, an anti-ET drug that is known to reduce the pathologic tremor in ?1(-/-) mice, was not effective for suppressing the potentiated tremor in ?1(-/-)/?(1G)(-/-) mice. In addition, ?1(-/-)/?(1G)(-/-) mice showed an age-dependent loss of cerebellar Purkinje neurons. These results suggest that ?1(-/-)/?(1G)(-/-) mice are a novel mouse model for a distinct subtype of ET in human and that Ca(V)3.1 T-type Ca(2+) channels play a role in motor coordination under pathological conditions.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
1090-2104
|
pubmed:author | |
pubmed:copyrightInfo |
Copyright © 2011 Elsevier Inc. All rights reserved.
|
pubmed:issnType |
Electronic
|
pubmed:day |
24
|
pubmed:volume |
410
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
19-23
|
pubmed:meshHeading |
pubmed-meshheading:21621520-Age Factors,
pubmed-meshheading:21621520-Animals,
pubmed-meshheading:21621520-Calcium Channels, T-Type,
pubmed-meshheading:21621520-Cerebellar Ataxia,
pubmed-meshheading:21621520-Cerebellum,
pubmed-meshheading:21621520-Disease Models, Animal,
pubmed-meshheading:21621520-Essential Tremor,
pubmed-meshheading:21621520-Humans,
pubmed-meshheading:21621520-Mice,
pubmed-meshheading:21621520-Mice, Knockout,
pubmed-meshheading:21621520-Models, Genetic,
pubmed-meshheading:21621520-Motor Activity,
pubmed-meshheading:21621520-Purkinje Cells,
pubmed-meshheading:21621520-Receptors, GABA-A
|
pubmed:year |
2011
|
pubmed:articleTitle |
Lack of CaV3.1 channels causes severe motor coordination defects and an age-dependent cerebellar atrophy in a genetic model of essential tremor.
|
pubmed:affiliation |
Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Republic of Korea.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|