PLC beta 4-independent Ca2+ rise via muscarinic receptors in the mouse suprachiasmatic nucleus

Neuroreport. 2000 Apr 7;11(5):907-12. doi: 10.1097/00001756-200004070-00002.

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-beta (PLC-beta) families that couple to muscarinic acetylcholine receptors (mAChR) and demonstrated the expression of PLC-beta 1 and beta 4 in the mouse SCN. Ca2+ imaging analysis indicated that the MI-mAChR antagonist, pirenzepine blocked carbachol-induced Ca2+ elevation in the SCN and the response was equivalent between the wild type and the PLC-beta 4-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-beta 1 but not PLC-beta 4 was involved in the mAChR-mediated Ca2+ signaling in the SCN.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Carbachol / pharmacology
  • Cholinergic Fibers / metabolism
  • Circadian Rhythm / physiology
  • Immunohistochemistry
  • Isoenzymes / metabolism*
  • Mice
  • Mice, Knockout
  • Motor Activity / drug effects
  • Motor Activity / physiology
  • Neurons / metabolism
  • Neurons / physiology
  • Phospholipase C beta
  • Receptors, Muscarinic / drug effects
  • Receptors, Muscarinic / metabolism*
  • Receptors, Muscarinic / physiology*
  • Suprachiasmatic Nucleus / metabolism*
  • Suprachiasmatic Nucleus / physiology*
  • Type C Phospholipases / metabolism*

Substances

  • Isoenzymes
  • Receptors, Muscarinic
  • Carbachol
  • Type C Phospholipases
  • Phospholipase C beta
  • Plcb4 protein, mouse
  • Calcium