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J Neurophysiol (February 4, 2004). doi:10.1152/jn.01148.2003
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Submitted on December 1, 2003
Accepted on January 29, 2004

Enhanced long-term potentiation during aging is masked by processes involving intracellular calcium stores

Ashok Kumar and Thomas Foster*

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

The contribution of Ca2+ release from intracellular Ca2+ stores (ICS) for regulation of synaptic plasticity thresholds during aging was investigated in hippocampal slices of aged (22-24 month) and young adult (5-8 month) male Fischer 344 rats. Inhibition of Ca2+-induced Ca2+ release by thapsigargin, cyclopiazonic acid (CPA), or ryanodine during pattern stimulation near the threshold for synaptic modification (5 Hz, 900 pulses) selectively induced long-term potentiation (LTP) to CA1 Schaffer collateral synapses of aged rats. Increased synaptic strength was specific to test pathways and blocked by AP-5. Intracellular recordings demonstrated that ICS plays a role in the augmentation of the afterhyperpolarization (AHP) in aged rats. The decrease in the AHP by ICS inhibition was reversed by the L-channel agonist, Bay K8644. Under conditions of ICS inhibition and a Bay K8644 mediated enhancement of the AHP, pattern stimulation failed to induce LTP consistent with the idea that the AHP amplitude shapes the threshold for LTP-induction. Finally, ICS inhibition was associated with an increase in the N-methyl-D-aspartate (NMDA) receptor component of synaptic transmission in aged animals. This increase in the synaptic response was blocked by the calcineurin inhibitor FK506. The results reveal an age-related increase in susceptibility to LTP-induction which is normally inhibited by ICS and suggest that the age-related shift in Ca2+ regulation and Ca2+-dependent synaptic plasticity is coupled to changes in cell excitability and NMDA receptor function through ICS.




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