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Proc Natl Acad Sci U S A. 2007 Nov 6;104(45):17819-24. Epub 2007 Oct 29.

Gamma-band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice.

Author information

1
Department of Physiology and Neuroscience, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA. llinar01@med.nyu.edu

Abstract

Thalamocortical in vivo and in vitro function was studied in mice lacking P/Q-type calcium channels (Cav2.1), in which N-type calcium channels (Cav2.2) supported central synaptic transmission. Unexpectedly, in vitro patch recordings from thalamic neurons demonstrated no gamma-band subthreshold oscillation, and voltage-sensitive dye imaging demonstrated an absence of cortical gamma-band-dependent columnar activation involving cortical inhibitory interneuron activity. In vivo electroencephalogram recordings showed persistent absence status and a dramatic reduction of gamma-band activity. Pharmacological block of T-type calcium channels (Cav3), although not noticeably affecting normal control animals, left the knockout mice in a coma-like state. Hence, although N-type calcium channels can rescue P/Q-dependent synaptic transmission, P/Q calcium channels are essential in the generation of gamma-band activity and resultant cognitive function.

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PMID:
17968008
PMCID:
PMC2077027
DOI:
10.1073/pnas.0707945104
[Indexed for MEDLINE]
Free PMC Article

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