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dc.contributor.authorWang, Louisa M.
dc.contributor.authorSuthana, Nanthia A.
dc.contributor.authorChaudhury, Dipesh
dc.contributor.authorWeaver, David R.
dc.contributor.authorColwell, Christopher S.
dc.date2022-08-11T08:09:30.000
dc.date.accessioned2022-08-23T16:33:09Z
dc.date.available2022-08-23T16:33:09Z
dc.date.issued2005-11-01
dc.date.submitted2012-05-24
dc.identifier.citationEur J Neurosci. 2005 Nov;22(9):2231-7. <a href="http://dx.doi.org/10.1111/j.1460-9568.2005.04408.x">Link to article on publisher's site</a>
dc.identifier.issn0953-816X (Linking)
dc.identifier.doi10.1111/j.1460-9568.2005.04408.x
dc.identifier.pmid16262661
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38036
dc.description.abstractThe goal of this study is to investigate the effect of the hormone melatonin on long-term potentiation and excitability measured by stimulating the Schaffer collaterals and recording the field excitatory postsynaptic potential from the CA1 dendritic layer in hippocampal brain slices from mice. Application of melatonin produced a concentration-dependent inhibition of the induction of long-term potentiation, with a concentration of 100 nm producing an approximately 50% inhibition of long-term potentiation magnitude. Long-duration melatonin treatments of 6 h were also effective at reducing the magnitude of long-term potentiation. Melatonin (100 nm) did not alter baseline evoked responses or paired-pulse facilitation recorded at this synapse. The inhibitory actions of melatonin were prevented by application of the melatonin (MT) receptor antagonist luzindole as well as the MT2 receptor subtype antagonist 4-phenyl-2-propionamidotetraline. These inhibitory actions of melatonin were lost in mice deficient in MT2 receptors but not those deficient in MT1 receptors. In addition, application of the protein kinase A inhibitor H-89 both mimicked the effects of melatonin and precluded further inhibition by melatonin. Finally, the application an activator of adenylyl cyclase, forskolin, overcame the inhibitory effects of melatonin on LTP without affecting the induction of long-term potentiation on its own. These results suggest that hippocampal synaptic plasticity may be constrained by melatonin through a mechanism involving MT2-receptor-mediated regulation of the adenylyl cyclase-protein kinase A pathway.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=16262661&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581482/pdf/nihms73182.pdf
dc.subjectAnimals
dc.subjectAntioxidants
dc.subjectDose-Response Relationship, Drug
dc.subjectDose-Response Relationship, Radiation
dc.subjectElectric Stimulation
dc.subjectExcitatory Postsynaptic Potentials
dc.subjectHippocampus
dc.subjectIsoquinolines
dc.subjectLong-Term Potentiation
dc.subjectMale
dc.subjectMelatonin
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectProtein Kinase Inhibitors
dc.subjectReceptor, Melatonin, MT1
dc.subjectReceptor, Melatonin, MT2
dc.subjectSulfonamides
dc.subjectSynaptic Transmission
dc.subjectTryptamines
dc.subjectNeuroscience and Neurobiology
dc.titleMelatonin inhibits hippocampal long-term potentiation
dc.typeJournal Article
dc.source.journaltitleThe European journal of neuroscience
dc.source.volume22
dc.source.issue9
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/neurobiology_pp/69
dc.identifier.contextkey2911184
html.description.abstract<p>The goal of this study is to investigate the effect of the hormone melatonin on long-term potentiation and excitability measured by stimulating the Schaffer collaterals and recording the field excitatory postsynaptic potential from the CA1 dendritic layer in hippocampal brain slices from mice. Application of melatonin produced a concentration-dependent inhibition of the induction of long-term potentiation, with a concentration of 100 nm producing an approximately 50% inhibition of long-term potentiation magnitude. Long-duration melatonin treatments of 6 h were also effective at reducing the magnitude of long-term potentiation. Melatonin (100 nm) did not alter baseline evoked responses or paired-pulse facilitation recorded at this synapse. The inhibitory actions of melatonin were prevented by application of the melatonin (MT) receptor antagonist luzindole as well as the MT2 receptor subtype antagonist 4-phenyl-2-propionamidotetraline. These inhibitory actions of melatonin were lost in mice deficient in MT2 receptors but not those deficient in MT1 receptors. In addition, application of the protein kinase A inhibitor H-89 both mimicked the effects of melatonin and precluded further inhibition by melatonin. Finally, the application an activator of adenylyl cyclase, forskolin, overcame the inhibitory effects of melatonin on LTP without affecting the induction of long-term potentiation on its own. These results suggest that hippocampal synaptic plasticity may be constrained by melatonin through a mechanism involving MT2-receptor-mediated regulation of the adenylyl cyclase-protein kinase A pathway.</p>
dc.identifier.submissionpathneurobiology_pp/69
dc.contributor.departmentWeaver Lab
dc.contributor.departmentNeurobiology
dc.source.pages2231-7


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