Age-related synapse loss in hippocampal CA3 is not reversed by caloric restriction

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buir.contributor.authorAdams, Michelle M.
dc.citation.epage382en_US
dc.citation.issueNumber2en_US
dc.citation.spage373en_US
dc.citation.volumeNumber171en_US
dc.contributor.authorAdams, Michelle M.en_US
dc.contributor.authorDonohue, H. S.en_US
dc.contributor.authorLinville, M. C.en_US
dc.contributor.authorIversen, E. A.en_US
dc.contributor.authorNewton, I. G.en_US
dc.contributor.authorBechtold, J. K. B.en_US
dc.date.accessioned2016-02-08T09:55:51Z
dc.date.available2016-02-08T09:55:51Z
dc.date.issued2010en_US
dc.departmentDepartment of Psychologyen_US
dc.departmentAysel Sabuncu Brain Research Center (BAM)en_US
dc.description.abstractCaloric restriction (CR) is a reduction of total caloric intake without a decrease in micronutrients or a disproportionate reduction of any one dietary component. While CR attenuates age-related cognitive deficits in tasks of hippocampal-dependent memory, the cellular mechanisms by which CR improves this cognitive decline are poorly understood. Previously, we have reported age-related decreases in key synaptic proteins in the CA3 region of the hippocampus that are stabilized by lifelong CR. In the present study, we examined possible age-related changes in the functional microcircuitry of the synapses in the stratum lacunosum-moleculare (SL-M) of the CA3 region of the hippocampus, and whether lifelong CR might prevent these age-related alterations. We used serial electron microscopy to reconstruct and classify SL-M synapses and their postsynaptic spines. We analyzed synapse number and size as well as spine surface area and volume in young (10 months) and old (29 months) ad libitum fed rats and in old rats that were calorically restricted from 4 months of age. We limited our analysis to SL-M because previous work demonstrated age-related decreases in synaptophysin confined to this specific layer and region of the hippocampus. The results revealed an age-related decrease in macular axo-spinous synapses that was not reversed by CR that occurred in the absence of changes in the size of synapses or spines. Thus, the benefits of CR for CA3 function and synaptic plasticity may involve other biological effects including the stabilization of synaptic proteins levels in the face of age-related synapse loss. © 2010 IBRO.en_US
dc.identifier.doi10.1016/j.neuroscience.2010.09.022en_US
dc.identifier.eissn1873-7544
dc.identifier.issn0306-4522
dc.identifier.urihttp://hdl.handle.net/11693/22128
dc.language.isoEnglishen_US
dc.publisherPergamon Pressen_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.neuroscience.2010.09.022en_US
dc.source.titleSynapsesen_US
dc.subjectDietary restrictionen_US
dc.subjectElectron microscopyen_US
dc.subjectHippocampusen_US
dc.subjectRaten_US
dc.subjectSerial reconstructionen_US
dc.titleAge-related synapse loss in hippocampal CA3 is not reversed by caloric restrictionen_US
dc.typeArticleen_US
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