Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 102, Issue 5, Pages 1743-1748Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0409644102
Keywords
insomnia; alpha 1G; thalamus; arousal; Cre recombinase
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Funding
- NHLBI NIH HHS [P50 HL060292, P01-HL60292] Funding Source: Medline
- NIMH NIH HHS [R01 MH062589, P50-MH58880, R01-MH62589, P50 MH058880, K08 MH001844] Funding Source: Medline
- NINDS NIH HHS [R01 NS032925, R01-NS32925] Funding Source: Medline
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it has long been suspected that sensory signal transmission is inhibited in the mammalian brain during sleep. We hypothesized that Ca(v)3.1 T-type Ca2+ channel currents inhibit thalamic sensory transmission to promote sleep. We found that T-type Ca2+ channel activation caused prolonged inhibition (>9 s) of action-potential firing in thalamic projection neurons of WT but not Ca(v)3.1 knockout mice. Inhibition occurred with synaptic transmission blocked and required an increase of intracellular Ca2+. Furthermore, focal deletion of the gene encoding Ca(v)3.1 from the rostral-midline thalamus by using Cre/loxP recombination led to frequent and prolonged arousal, which fragmented and reduced sleep. Interestingly, sleep was not disturbed when Ca(v)3.1 was deleted from cortical pyramidal neurons. These findings support the hypothesis that thalamic T-type Ca2+ channels are required to block transmission of arousal signals through the thalamus and to stabilize sleep.
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