Effect of adenosine-induced changes in presynaptic release probability on long-term potentiation in the hippocampal CA1 region.
In the present study some characteristics of long-term potentiation (LTP) in the hippocampal CA1 region were examined under different conditions of transmitter release. Adenosine A1 agonist/antagonists, or in some instances changes in the extracellular calcium/magnesium ratio, were used to alter release probability. The overall LTP time course (onset latency, growth phase, and subsequent decay for both the non-NMDA and NMDA receptor-mediated EPSPs) following a brief tetanus was essentially the same over an almost 10-fold variation in release probability (measured as change in field EPSP magnitude). The major difference observed was a faster initial decay of LTP evoked at low levels of release probability, possibly related to impaired induction conditions. It was also observed that LTP induced at one level of release probability occluded that induced at a lower (or higher) level, and that changes in release probability induced by adenosine agonist/antagonists affected potentiated and "naive" EPSPs to an equal extent. Taken together, these data do not provide support for the notion of different locations for LTP expression at different conditions of release probability. The results are also more compatible with the notion of a single, rather than several, expression mechanism(s) within the first hour of LTP in the hippocampal CA1 region.[1]References
- Effect of adenosine-induced changes in presynaptic release probability on long-term potentiation in the hippocampal CA1 region. Asztely, F., Xiao, M.Y., Wigström, H., Gustafsson, B. J. Neurosci. (1994) [Pubmed]
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