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dc.contributor.authorvon Gall, Charlotte
dc.contributor.authorWeaver, David R.
dc.date2022-08-11T08:09:30.000
dc.date.accessioned2022-08-23T16:33:00Z
dc.date.available2022-08-23T16:33:00Z
dc.date.issued2008-03-01
dc.date.submitted2012-05-24
dc.identifier.citationNeurobiol Aging. 2008 Mar;29(3):464-70. Epub 2006 Nov 22. <a href="http://dx.doi.org/10.1016/j.neurobiolaging.2006.10.015">Link to article on publisher's site</a>
dc.identifier.issn0197-4580 (Linking)
dc.identifier.doi10.1016/j.neurobiolaging.2006.10.015
dc.identifier.pmid17123666
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38004
dc.description.abstractMelatonin modulates circadian rhythms via the hypothalamic suprachiasmatic nucleus (SCN). One of the most robust assays for SCN melatonin receptor activation in mice is the inhibition of PACAP-induced phosphorylation of the transcription factor Ca(2+)/cAMP responsive element binding protein (CREB). To assess the effect of aging on responsiveness to melatonin, SCN slices from mice of different ages were prepared and treated with PACAP alone or PACAP plus melatonin. CREB phosphorylation state was assessed by immunohistochemistry. In SCN slices from young (2-4-month-old) mice, melatonin reduced the level of phospho-CREB immunoreactivity following PACAP treatment in a dose-dependent manner. In SCN slices from aged mice (19-22 months of age), PACAP alone induced comparable levels of phospho-CREB, but melatonin treatment failed to inhibit the PACAP-induced CREB phosphorylation. The results indicate an age-related loss of sensitivity to melatonin in the SCN. The findings are discussed in the context of the impact of endogenous and exogenous melatonin on sleep in elderly humans.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17123666&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.neurobiolaging.2006.10.015
dc.subjectAge Factors
dc.subject*Aging
dc.subjectAnimals
dc.subjectCREB-Binding Protein
dc.subjectDrug Interactions
dc.subjectMelatonin
dc.subjectMetallothionein
dc.subjectMice
dc.subjectMice, Knockout
dc.subjectNeurotransmitter Agents
dc.subjectPhosphorylation
dc.subjectPituitary Adenylate Cyclase-Activating Polypeptide
dc.subjectSuprachiasmatic Nucleus
dc.subjectNeuroscience and Neurobiology
dc.titleLoss of responsiveness to melatonin in the aging mouse suprachiasmatic nucleus
dc.typeJournal Article
dc.source.journaltitleNeurobiology of aging
dc.source.volume29
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/neurobiology_pp/38
dc.identifier.contextkey2911153
html.description.abstract<p>Melatonin modulates circadian rhythms via the hypothalamic suprachiasmatic nucleus (SCN). One of the most robust assays for SCN melatonin receptor activation in mice is the inhibition of PACAP-induced phosphorylation of the transcription factor Ca(2+)/cAMP responsive element binding protein (CREB). To assess the effect of aging on responsiveness to melatonin, SCN slices from mice of different ages were prepared and treated with PACAP alone or PACAP plus melatonin. CREB phosphorylation state was assessed by immunohistochemistry. In SCN slices from young (2-4-month-old) mice, melatonin reduced the level of phospho-CREB immunoreactivity following PACAP treatment in a dose-dependent manner. In SCN slices from aged mice (19-22 months of age), PACAP alone induced comparable levels of phospho-CREB, but melatonin treatment failed to inhibit the PACAP-induced CREB phosphorylation. The results indicate an age-related loss of sensitivity to melatonin in the SCN. The findings are discussed in the context of the impact of endogenous and exogenous melatonin on sleep in elderly humans.</p>
dc.identifier.submissionpathneurobiology_pp/38
dc.contributor.departmentWeaver Lab
dc.contributor.departmentNeurobiology
dc.source.pages464-70


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