Presynaptic ultrastructural correlates of long-term potentiation in the CA1 subfield of the hippocampus.
To determine if long-term potentiation (LTP) is accompanied by changes in the ultrastructural distribution of calcium within presynaptic terminals, calcium was localized at the electron microscopic level using an oxalate/pyroantimonate histochemical technique. Following the induction of LTP at the Schaffer collateral/commissural synapses in the CA1 subfield of the rat hippocampal slice, there was a significant decrease (30%) in the percentage of synaptic vesicles containing calcium deposits. This effect could be accounted for by both a significant reduction in the average number of calcium deposit-bearing vesicles and a significant increase in the average number of synaptic vesicles per terminal profile in slices that displayed LTP. These changes persisted for at least one hour following the induction of LTP and were not observed in slices that received high-frequency stimulation in the presence of the N-methyl-D-aspartate (NMDA) receptor antagonist, 2-amino-5-phosphonovaleric acid (APV, 50 microM), which blocked LTP. These data suggest that LTP may be accompanied by long-term changes in intraterminal calcium homeostasis and the number of synaptic vesicles. These effects may be related to the reported increase in transmitter release following the induction of LTP.[1]References
- Presynaptic ultrastructural correlates of long-term potentiation in the CA1 subfield of the hippocampus. Meshul, C.K., Hopkins, W.F. Brain Res. (1990) [Pubmed]
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