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Shift in Induction Mechanisms Underlies an Age-Dependent Increase in DHPG-Induced Synaptic Depression at CA3–CA1 Synapses

Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, Florida

Submitted 8 May 2007; accepted in final form 24 September 2007

Several forms of log-term synaptic plasticity have been identified and the mechanisms for induction and expression of synaptic modifications change over development and maturation. The present study examines age-related changes in the induction of group I metabotropic receptor selective agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) induced long-term synaptic depression (DHPG-LTD) at CA3–CA1 synapses. The results demonstrate that the magnitude of DHPG-LTD is enhanced in male aged Fischer 344 rats compared with young adults. The role of mGluR1 in the induction of DHPG-LTD was increased with advanced age and, in contrast to young adults, induction involved a significant contribution of NMDA receptors and L-type Ca²⁺ channels. Moreover, the protein tyrosine phosphatase inhibitor sodium orthovanadate significantly attenuated DHPG-LTD only in young adults. The expression of DHPG-LTD in aged animals was dependent on protein synthesis and the enhanced expression was associated with an increase in paired-pulse facilitation. The results provide evidence that DHPG-LTD is one of the few forms of synaptic plasticity that increases with advanced age and suggest that DHPG-LTD may contribute to age-related changes in hippocampal function.

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