AI Article Synopsis
- Research suggests that sensory signal transmission in the mammalian brain is inhibited during sleep, specifically through Cav3.1 T-type Ca2+ channels.
- The activation of these channels leads to prolonged inhibition of action-potential firing in thalamic neurons, essential for promoting sleep.
- Deleting Cav3.1 in specific brain areas resulted in increased arousal and disrupted sleep patterns, supporting the idea that these channels help stabilize sleep by blocking arousal signals.
Article Abstract
It has long been suspected that sensory signal transmission is inhibited in the mammalian brain during sleep. We hypothesized that Cav3.1 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 Cav3.1 knockout mice. Inhibition occurred with synaptic transmission blocked and required an increase of intracellular Ca2+. Furthermore, focal deletion of the gene encoding Cav3.1 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 Cav3.1 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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC547889 | PMC |
| http://dx.doi.org/10.1073/pnas.0409644102 | DOI Listing |
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