Molecular components and mechanism of adrenergic signal transduction in mammalian pineal gland: regulation of melatonin synthesis.

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dc.contributor.authorGupta, B B Pen_US
dc.contributor.authorSpessert, Ren_US
dc.contributor.authorVollrath, Len_US
dc.date.accessioned2009-05-28T12:42:30Z
dc.date.available2009-05-28T12:42:30Z
dc.date.issued2005-02-24en_US
dc.description371 references.en_US
dc.description.abstractRhythmic neural outputs from the hypothalamic suprachiasmatic nucleus (SCN), which programme the rhythmic release of norepinephrine (NE) from intrapineal nerve fibers, regulate circadian rhythm of melatonin synthesis. Increased secretion of NE with the onset of darkness during the first half of night stimulates melatonin synthesis by several folds. NE binds to both alpha1- and beta-adrenergic receptors present on the pinealocyte membrane and initiates adrenergic signal transduction via cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) generating pathways. The NE-induced adrenergic signal transduction switches 'on' melatonin synthesis during the early hours of night by stimulating expression of the rate-limiting enzyme of melatonin synthesis, N-acetyltransferase (AA-NAT) via cAMP-protein kinase A (PKA)-cAMP response element binding protein (CREB)-cAMP response element (CRE) pathway as well as by increasing AA-NAT activity via cAMP-PKA-14-3-3 protein pathway. Simultaneously, adrenergically-induced expression of inducible cAMP early repressor (ICER) negatively regulates aa-nat gene expression and controls the amplitude of melatonin rhythm. In the second half of night, increased release of acetylcholine from central pinealopetal projections, inhibition of NE secretion by SCN, withdrawal of adrenergic inputs and reversal of events that took place in the first half lead to switching 'off' of melatonin synthesis. Adrenergic signal transduction via cGMP-protein kinase G (PKG)-mitogen activated protein kinase (MAPK)-ribosomal S6 kinase (RSK) pathway also seems to be fully functional, but its role in modulation of melatonin synthesis remains unexplored. This article gives a critical review of information available on various components of the adrenergic signal transduction cascades involved in the regulation of melatonin synthesis.en_US
dc.description.affiliationEnvironmental Endocrinology Laboratory, Department of Zoology, North-Eastern Hill University, Shillong 793 022, India. gupta@nehu.ac.inen_US
dc.identifier.citationGupta BB, Spessert R, Vollrath L. Molecular components and mechanism of adrenergic signal transduction in mammalian pineal gland: regulation of melatonin synthesis. Indian Journal of Experimental Biology. 2005 Feb; 43(2): 115-49en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/58447
dc.language.isoengen_US
dc.source.urihttps://www.niscair.res.in/ScienceCommunication/ResearchJournals/rejour/ijeb/ijeb0.aspen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Membrane --metabolismen_US
dc.subject.meshCircadian Rhythm --physiologyen_US
dc.subject.meshMammalsen_US
dc.subject.meshMelatonin --biosynthesisen_US
dc.subject.meshPineal Gland --enzymologyen_US
dc.subject.meshReceptors, Adrenergic --metabolismen_US
dc.subject.meshSignal Transduction --physiologyen_US
dc.titleMolecular components and mechanism of adrenergic signal transduction in mammalian pineal gland: regulation of melatonin synthesis.en_US
dc.typeJournal Articleen_US
dc.typeReviewen_US
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