Show simple item record

dc.contributor.authorMolina, D. P.en_US
dc.contributor.authorAriwodola, O. J.en_US
dc.contributor.authorWeiner, J. L.en_US
dc.contributor.authorBechtold, J. K. B.en_US
dc.contributor.authorAdams, Michelle M.en_US
dc.date.accessioned2016-02-08T09:35:29Z
dc.date.available2016-02-08T09:35:29Z
dc.date.issued2013en_US
dc.identifier.issn0312-6307
dc.identifier.urihttp://hdl.handle.net/11693/20800
dc.description.abstractIn rats, as in humans, normal aging is characterized by a decline in hippocampal-dependent learning and memory, as well as in glutamatergic function. Both growth hormone (GH) and insulin-like growth factor-I (IGF-I) levels have been reported to decrease with age, and treatment with either GH or IGF-I can ameliorate age-related cognitive decline. Interestingly, acute GH and IGF-I treatments enhance glutamatergic synaptic transmission in the rat hippocampus of juvenile animals. However, whether this enhancement also occurs in old rats, when cognitive impairment is ameliorated by GH and IGF-I (des-IGF-I), remains to be determined. To address this issue, we used an in vitro CA1 hippocampal slice preparation and extracellular recording techniques to study the effects of acute application of GH and IGF-I on compound field excitatory postsynaptic potentials (fEPSPs), as well as AMPA- and NMDA-dependent fEPSPs, in young adult (10 months) and old (28 months) rats. The results indicated that both GH and IGF-I increased compound-, AMPA-and NMDA-dependent fEPSPs to a similar extent in slices from both age groups and that this augmentation was likely mediated via a postsynaptic mechanism. Initial characterization of the signaling cascades underlying these effects revealed that the GH-induced enhancement was not mediated by the JAK2 signaling element in either young adult or old rats but that the IGF-Iinduced enhancement involved a PI3K-mediated mechanism in old, but not young adults. The present findings are consistent with a role for a GH-or IGF-I-induced enhancement of glutamatergic transmission in mitigating age-related cognitive impairment in old rats. © 2012 American Aging Association.en_US
dc.language.isoEnglishen_US
dc.source.titleThe Ageen_US
dc.relation.isversionofhttp://dx.doi.org/10.1007/s11357-012-9460-4en_US
dc.subjectPlasticityen_US
dc.subjectPostsynapticen_US
dc.subjectPhosphorylationen_US
dc.subjectGlutamate receptorsen_US
dc.subjectCell signalingen_US
dc.titleGrowth hormone and insulin-like growth factor-I alter hippocampal excitatory synaptic transmission in young and old ratsen_US
dc.typeArticleen_US
dc.departmentDepartment of Psychologyen_US
dc.departmentAysel Sabuncu Brain Research Center (BAM)en_US
dc.citation.spage1575en_US
dc.citation.epage1587en_US
dc.citation.volumeNumber35en_US
dc.citation.issueNumber5en_US
dc.identifier.doi10.1007/s11357-012-9460-4en_US
dc.publisherAge Companyen_US
dc.contributor.bilkentauthorAdams, Michelle M.


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record