Siwek, Magdalena Elisabeth, Mueller, Ralf, Henseler, Christina, Broich, Karl, Papazoglou, Anna and Weiergraeber, Marco (2014). The Ca-V 2.3 R-Type Voltage-Gated Ca2+ Channel in Mouse Sleep Architecture. Sleep, 37 (5). S. 881 - 895. CARY: OXFORD UNIV PRESS INC. ISSN 1550-9109

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Abstract

Study Objectives: Voltage-gated Ca2+ channels (VGCCs) are key elements in mediating thalamocortical rhythmicity. Low-voltage activated (LVA) Ca(V)3 T-type Ca2+ channels have been related to thalamic rebound burst firing and to generation of non-rapid eye movement (NREM) sleep. High-voltage activated (HVA) Ca(V)1 L-type Ca2+ 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 Ca(V)2.3 Ca2+ channels, which are predominantly expressed in the reticular thalamic nucleus (RTN), still remains unclear. Recently, Ca(V)2.3(-/-) mice were reported to exhibit altered spike-wave discharge (SWD)/absence seizure susceptibility supported by the observation that Ca(V)2.3 mediated Ca2+ influx into RTN neurons can trigger small-conductance Ca2+-activated K+-channel type 2 (SK2) currents capable of maintaining thalamic burst activity. Based on these studies we investigated the role of Ca(V)2.3 R-type Ca2+ channels in rodent sleep. Methods: The role of Ca(V)2.3 Ca2+ channels was analyzed in Ca(V)2.3(-/-) 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: Ca(V)2.3 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 Ca(V)2.3(-/-) mice. Additional changes were observed for sleep stage transitions and EEG amplitudes. Furthermore, urethane-induced SWS mimicked spontaneous sleep results obtained from Ca(V)2.3 deficient mice. Quantitative Real-time PCR did not reveal changes in thalamic Ca(V)3 T-type Ca2+ channel expression. The detailed mechanisms of SWS increase in Ca(V)2.3(-/-) mice remain to be determined. Conclusions: Low-voltage activated Ca(V)2.3 R-type Ca2+ 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.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Siwek, Magdalena ElisabethUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Mueller, RalfUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Henseler, ChristinaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Broich, KarlUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Papazoglou, AnnaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Weiergraeber, MarcoUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-440291
DOI: 10.5665/sleep.3652
Journal or Publication Title: Sleep
Volume: 37
Number: 5
Page Range: S. 881 - 895
Date: 2014
Publisher: OXFORD UNIV PRESS INC
Place of Publication: CARY
ISSN: 1550-9109
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
DEPENDENT CALCIUM-CHANNELS; MICE LACKING; ANESTHETIC SENSITIVITIES; INTERNATIONAL-UNION; ABSENCE SEIZURES; THALAMIC NEURONS; PHARMACOLOGY; OSCILLATIONS; RESISTANCE; URETHANEMultiple languages
Clinical Neurology; NeurosciencesMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/44029

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