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Studies on synaptic potentiation in the hippocampus Goh, Joanne Wan Yoong


The present investigation was conducted on transversely sectioned rat hippocampal slices to examine the mechanisms involved in synaptic potentiation. Results indicate that long-term potentiation (LTP) induced by input tetanization requires extracellular Ca⁺⁺, because during the induction of LTP postsynaptic depolarization must accompany presynaptic activity (LTP could be induced by raised K⁺ [10 to 80 mM] in Ca⁺⁺-free medium). Since LTP (induced by raised K⁺) occurs in the absence of Ca⁺⁺ and, therefore, presumably in the near absence of transmitter release, N-methyl-D-aspartate (NMDA) receptor activation is not obligatory. Moreover, NMDA receptors appear not to be involved in the CA₃ area. A necessity for both pre- and postsynaptic depolarization also accounts for the need for co-stimulation of afferents for LTP induction. Associative potentiation was found not to require tetanic stimulation of the test input; single pulse activation of the test input (at 0.2 Hz) paired with tetanic trains to a conditioning input (presumably to the same postsynaptic neurones) could produce LTP. A short-term potentiation (STP), which resembled post-tetanic potentiation (PTP) in time course, could be induced in an associative fashion by conditioning tetanic trains (paired with single test stimuli), that were insufficient to produce LTP. In the absence of conditioning stimuli, interruption of a regular 0.2 Hz test input stimulation for 10 minutes disclosed a subsequent potentiation. This potentiation could be distinguished from associative potentiation in that it was not associated with a decrease in presynaptic terminal excitability. A decrease in presynaptic terminal excitability was characteristic of associative STP and LTP, and followed similar time courses. Since raised K⁺ reversed rather than accentuated the decreased excitability, it was concluded that it is not due to Na⁺ -inactivation and may be caused by a hyperpolarization which might also lead to an increase in evoked transmitter release. The hypothesis of Baudry and Lynch (1980a) that LTP is due to an increase in glutamate receptors seems unlikely; there was no increase in Na-independent glutamate binding sites (determined by the same method as used by Lynch et- al: [1982]) in association with LTP induced by a single brief 400 Hz (200 pulses) input tetanus. A decrease in the uptake of glutamate occurs with tetanic stimulation under conditions where there is no LTP (absence of Ca⁺⁺ and raised Mg⁺⁺ and Mn⁺⁺) and, therefore, does not appear to be a mechanism producing LTP.

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