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Tytuł pozycji:

Growth hormone and insulin-like growth factor-I alter hippocampal excitatory synaptic transmission in young and old rats.

Tytuł:
Growth hormone and insulin-like growth factor-I alter hippocampal excitatory synaptic transmission in young and old rats.
Autorzy:
Molina DP; Departments of Neurobiology and Anatomy, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC, 27157-1010, USA.
Ariwodola OJ
Weiner JL
Brunso-Bechtold JK
Adams MM
Źródło:
Age (Dordrecht, Netherlands) [Age (Dordr)] 2013 Oct; Vol. 35 (5), pp. 1575-87. Date of Electronic Publication: 2012 Aug 01.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: Dordrecht, The Netherlands ; Hingham, MA : Springer, c2005-
MeSH Terms:
Aging/*metabolism
Growth Hormone/*pharmacology
Hippocampus/*metabolism
Insulin-Like Growth Factor I/*pharmacology
Aging/drug effects ; Animals ; Cognition Disorders/drug therapy ; Cognition Disorders/metabolism ; Cognition Disorders/physiopathology ; Disease Models, Animal ; Hippocampus/drug effects ; Male ; Rats ; Rats, Inbred BN ; Rats, Inbred F344 ; Synaptic Transmission/drug effects
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Grant Information:
K01 AG027828 United States AG NIA NIH HHS; P01 AG011370 United States AG NIA NIH HHS; P01 AG11370 United States AG NIA NIH HHS; KO1 AG027828 United States AG NIA NIH HHS
Substance Nomenclature:
67763-96-6 (Insulin-Like Growth Factor I)
9002-72-6 (Growth Hormone)
Entry Date(s):
Date Created: 20120802 Date Completed: 20140520 Latest Revision: 20231106
Update Code:
20240104
PubMed Central ID:
PMC3776110
DOI:
10.1007/s11357-012-9460-4
PMID:
22851280
Czasopismo naukowe
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-I-induced 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.

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