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J Neurophysiol (September 26, 2007). doi:10.1152/jn.00514.2007
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Submitted on May 8, 2007
Accepted on September 24, 2007

Shift in induction mechanisms underlies an age-dependent increase in DHPG-induced synaptic depression at CA3-CA1 synapses

Ashok Kumar1* and Thomas C. Foster2

1 Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, Florida, United States
2 Neuroscience/Brain Institute, University of Florida, Gainesville, Florida, United States

* To whom correspondence should be addressed. E-mail: kash{at}mbi.ufl.edu.

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 (RS)-3,5-dihydroxyphenylglycine (DHPG) induced 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 to 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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D. R. Ireland and W. C. Abraham
Mechanisms of Group I mGluR-Dependent Long-Term Depression of NMDA Receptor-Mediated Transmission at Schaffer Collateral-CA1 Synapses
J Neurophysiol, March 1, 2009; 101(3): 1375 - 1385.
[Abstract] [Full Text] [PDF]


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