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http://purl.uniprot.org/citations/24790266http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Study objectives

Voltage-gated Ca(2+) channels (VGCCs) are key elements in mediating thalamocortical rhythmicity. Low-voltage activated (LVA) CaV 3 T-type Ca(2+) channels have been related to thalamic rebound burst firing and to generation of non-rapid eye movement (NREM) sleep. High-voltage activated (HVA) CaV 1 L-type Ca(2+) channels, on the opposite, favor the tonic mode of action associated with higher levels of vigilance. However, the role of the HVA Non-L-type CaV2.3 Ca(2+) channels, which are predominantly expressed in the reticular thalamic nucleus (RTN), still remains unclear. Recently, CaV2.3(-/-) mice were reported to exhibit altered spike-wave discharge (SWD)/absence seizure susceptibility supported by the observation that CaV2.3 mediated Ca(2+) influx into RTN neurons can trigger small-conductance Ca(2+)-activated K(+)-channel type 2 (SK2) currents capable of maintaining thalamic burst activity. Based on these studies we investigated the role of CaV2.3 R-type Ca(2+) channels in rodent sleep.

Methods

The role of CaV2.3 Ca(2+) channels was analyzed in CaV2.3(-/-) mice and controls in both spontaneous and artificial urethane-induced sleep, using implantable video-EEG radiotelemetry. Data were analyzed for alterations in sleep architecture using sleep staging software and time-frequency analysis.

Results

CaV2.3 deficient mice exhibited reduced wake duration and increased slow-wave sleep (SWS). Whereas mean sleep stage durations remained unchanged, the total number of SWS epochs was increased in CaV2.3(-/-) mice. Additional changes were observed for sleep stage transitions and EEG amplitudes. Furthermore, urethane-induced SWS mimicked spontaneous sleep results obtained from CaV2.3 deficient mice. Quantitative Real-time PCR did not reveal changes in thalamic CaV3 T-type Ca(2+) channel expression. The detailed mechanisms of SWS increase in CaV2.3(-/-) mice remain to be determined.

Conclusions

Low-voltage activated CaV2.3 R-type Ca(2+) channels in the thalamocortical loop and extra-thalamocortical circuitries substantially regulate rodent sleep architecture thus representing a novel potential target for pharmacological treatment of sleep disorders in the future."xsd:string
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http://purl.uniprot.org/citations/24790266http://purl.uniprot.org/core/author"Muller R."xsd:string
http://purl.uniprot.org/citations/24790266http://purl.uniprot.org/core/author"Papazoglou A."xsd:string
http://purl.uniprot.org/citations/24790266http://purl.uniprot.org/core/author"Weiergraber M."xsd:string
http://purl.uniprot.org/citations/24790266http://purl.uniprot.org/core/author"Broich K."xsd:string
http://purl.uniprot.org/citations/24790266http://purl.uniprot.org/core/author"Henseler C."xsd:string
http://purl.uniprot.org/citations/24790266http://purl.uniprot.org/core/author"Siwek M.E."xsd:string
http://purl.uniprot.org/citations/24790266http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24790266http://purl.uniprot.org/core/name"Sleep"xsd:string
http://purl.uniprot.org/citations/24790266http://purl.uniprot.org/core/pages"881-892"xsd:string
http://purl.uniprot.org/citations/24790266http://purl.uniprot.org/core/title"The CaV2.3 R-type voltage-gated Ca2+ channel in mouse sleep architecture."xsd:string
http://purl.uniprot.org/citations/24790266http://purl.uniprot.org/core/volume"37"xsd:string
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