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      • Department of Psychology
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      Growth hormone and insulin-like growth factor-I alter hippocampal excitatory synaptic transmission in young and old rats

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      Author(s)
      Molina, D. P.
      Ariwodola, O. J.
      Weiner, J. L.
      Bechtold, J. K. B.
      Adams, Michelle M.
      Date
      2013
      Source Title
      The Age
      Print ISSN
      0312-6307
      Publisher
      Age Company
      Volume
      35
      Issue
      5
      Pages
      1575 - 1587
      Language
      English
      Type
      Article
      Item Usage Stats
      148
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      108
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      Abstract
      In 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.
      Keywords
      Plasticity
      Postsynaptic
      Phosphorylation
      Glutamate receptors
      Cell signaling
      Permalink
      http://hdl.handle.net/11693/20800
      Published Version (Please cite this version)
      http://dx.doi.org/10.1007/s11357-012-9460-4
      Collections
      • Aysel Sabuncu Brain Research Center (BAM) 213
      • Department of Psychology 191
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