Universität zu Köln

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:	Creators Email ORCID ORCID Put Code Siwek, Magdalena Elisabeth UNSPECIFIED UNSPECIFIED UNSPECIFIED Mueller, Ralf UNSPECIFIED UNSPECIFIED UNSPECIFIED Henseler, Christina UNSPECIFIED UNSPECIFIED UNSPECIFIED Broich, Karl UNSPECIFIED UNSPECIFIED UNSPECIFIED Papazoglou, Anna UNSPECIFIED UNSPECIFIED UNSPECIFIED Weiergraeber, Marco UNSPECIFIED UNSPECIFIED UNSPECIFIED
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:	Keywords Language DEPENDENT CALCIUM-CHANNELS; MICE LACKING; ANESTHETIC SENSITIVITIES; INTERNATIONAL-UNION; ABSENCE SEIZURES; THALAMIC NEURONS; PHARMACOLOGY; OSCILLATIONS; RESISTANCE; URETHANE Multiple languages Clinical Neurology; Neurosciences Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/44029