γ-Band deficiency and abnormal thalamocortical activity in P/Q-type channel mutant mice
- *Department of Physiology and Neuroscience, New York University School of Medicine, 550 First Avenue, New York, NY 10016;
- ‡Center for Neural Science, Korea Institute of Science and Technology, Seoul 136-791, Korea;
- §Department of Neuroscience, University of Science and Technology, Daejon 305-333, Korea; and
- ¶Laboratotio de Fisiología y Biología Molecular, Instituto de Fisiología, Biología Molecular y Neurociencias, Universidad de Buenos Aires–Consejo Nacional de Investigaciones Científicas y Técnicas de Argentina, Ciudad Universitaria, C1428EHA Buenos Aires, Argentina
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Contributed by Rodolfo R. Llinas, September 4, 2007 (received for review June 7, 2007)
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 γ-band subthreshold oscillation, and voltage-sensitive dye imaging demonstrated an absence of cortical γ-band-dependent columnar activation involving cortical inhibitory interneuron activity. In vivo electroencephalogram recordings showed persistent absence status and a dramatic reduction of γ-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 γ-band activity and resultant cognitive function.
Footnotes
- †To whom correspondence may be addressed. E-mail: llinar01{at}med.nyu.edu or heesup.shin{at}gmail.com
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Author contributions: R.R.L. designed research; R.R.L., S.C., and F.J.U. performed research; H.-S.S. contributed new reagents/analytic tools; R.R.L., S.C., and F.J.U. analyzed data; and R.R.L., F.J.U., and H.-S.S. wrote the paper.
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The authors declare no conflict of interest.
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Freely available online through the PNAS open access option.
- © 2007 by The National Academy of Sciences of the USA
