RHYTHMSPLC β4-independent Ca2+ rise via muscarinic receptors in the mouse suprachiasmatic nucleusIkeda, Masayuki1,5,6; Sugiyama, Takashi2; Suzuki, Kaoru2; Moriya, Takahiro1; Shibata, Shigenobu3; Katsuki, Motoya4; Allen, Charles N.5; Yoshioka, Tohru1,2Author Information 1Advanced Research Center for Human Sciences, School of Human Sciences, Waseda University, 2-579-15 Mikajima, Tokorozawa, Saitama 359-1192 2Department of Molecular Neurobiology, School of Human Sciences, Waseda University, 2-579-15 Mikajima, Tokorozawa, Saitama 359-1192 3Department of Pharmacology and Brain Science, School of Human Sciences, Waseda University, 2-579-15 Mikajima, Tokorozawa, Saitama 359-1192 4Department of DNA Biology and Embryo Engineering, Research Center of Animal Models for Human Diseases, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan 5Center for Research on Occupational and Environmental Toxicology, Oregon Health Sciences University, 3181 Sam Jackson Park Road, L606, Portland, OR 97201-3098, USA 6Corresponding Author: Masayuki Ikeda and Address: Center for Research on Occupational and Environmental Toxicology, Oregon Health Sciences University, 3181 Sam Jackson Park Road, L606, Portland, OR 97201-3098, USA Acknowledgements: This work is supported by a grant from Research for the Future (RFTF) program 69L00310 from Japan Society for the Promotion of Science to T.Y. and a grant from the National Institute of Health (NS036607) to C.N.A. Received 10 November 1999; accepted 15 January 2000 NeuroReport: April 7, 2000 - Volume 11 - Issue 5 - p 907-912 Buy Abstract Cholinergic regulation of the suprachiasmatic nucleus (SCN) has been extensively studied although the intracellular signaling mechanisms are not well understood. We examined immunostaining for phospholipase C-β (PLC-β) families that couple to muscarinic acetylcholine receptors (mAChR) and demonstrated the expression of PLC-β1 and β4 in the mouse SCN. Ca2+ imaging analysis indicated that the M1-mAChR antagonist, pirenzepine blocked carbachol-induced Ca2+ elevation in the SCN and the response was equivalent between the wild type and the PLC-β4-knockout mice. In addition, the knockout mice displayed locomotor and temperature rhythms coupling to 24 h light/dark cycles. Therefore, it was proposed that PLC-β1 but not PLC-β4 was involved in the mAChR-mediated Ca2+ signaling in the SCN. © 2000 Lippincott Williams & Wilkins, Inc.