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      Pineal Muscarinic Phosphoinositide Responses: Age-Associated Sensitization, Agonist-Induced Desensitization and Increase in Melatonin Release from Cultured Pineal Glands

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          Abstract

          Regulation of phosphoinositide (PI) signaling through the muscarinic cholinergic receptors (mAChRs) and their possible role were explored in the rat pineal gland. A sensitization of the PI signaling pathway was seen with advancing age. Binding of the mAChR ligand [N-methyl-<sup>3</sup>H]scopolamine to pineal sections, as detected by autoradiography, significantly decreased with advancing age and thus negatively correlated with the gland’s ability to respond to cholinergic stimulus. The cholinergic agonist carbachol induced a time-dependent desensitization of the muscarinic PI signaling after 2 h of pretreatment in vitro (43 and 61 % dampening of the PI response after 2 and 11 h pretreatment, respectively). This homologous desensitization was not mimicked by forskolin or phorbol esters, suggesting that proteins kinases A and C were not involved. Carbachol stimulation of the pineal glands in vitro increased melatonin release 2-fold, an effect quantitatively similar to that seen after adenylyl cyclase activation. Carbachol failed, however, to affect pineal cAMP levels. These results suggest that the PI signaling through pineal mAChRs is desensitized in young rats, possibly due to higher exposure to endogenous acetylcholine. Thus acetylcholine might play a prominent role in the developing gland. Moreover, acetylcholine could modulate melatonin release from the adult pineal gland in vivo.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1992
          1992
          07 April 2008
          : 55
          : 5
          : 492-499
          Affiliations
          aSection on Pharmacology, Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Md., USA; bDepartment of Physiology, University of Oulu, Finland
          Article
          126162 Neuroendocrinology 1992;55:492–499
          10.1159/000126162
          1316561
          © 1992 S. Karger AG, Basel

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          Page count
          Pages: 8
          Categories
          Original Paper

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