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UBC Theses and Dissertations

Long-lasting potentiation and depression of synaptic responses in the hippocampus Goh, Joanne Wan Yoong


Tetanic stimulations when applied to the Schaffer collaterals or the commissural input to CA₁ neurones in the mammalian hippocampus results in a long-lasting potentiation (LLP) of synaptic transmission across the tetanized synapse (Andersen et al., 1977; Schwartzkroin and Wester 1975). The induction of LLP is dependent on the extracellular Ca⁺⁺ concentration (Dunwiddie and Lynch, 1979; Wigstrom et al., 1979) but whether it is generated pre- and/or postsynaptically is at present unresolved. Transient homo- and heterosynaptic depressions of the CA₁ population spike have been reported following low frequency (I-20 Hz) tetani to hippocampal inputs (Lynch et al., 1977; Alger et al., 1978) which precede the observation of homosynaptic LLP (Dunwiddie and Lynch, 1978). The present studies were conducted to 1) test the hypothesis of Baudry and Lynch (1980a) who think that LLP can be explained postsynaptically by a Ca⁺⁺ dependent increase in the number of transmitter receptors; 2) examine the effects of verapamil (a Ca⁺⁺ antagonist that blocks CA₁ neuronal Ca⁺⁺ currents [Griffith and Brown, 1982] without interfering with transmitter release [Nachshen and Blaustein, 1979]) on the induction of LLP and homo- and heterosynaptic depressions; 3) investigate the Ca⁺⁺ dependence of a decrease in presynaptic terminal excitability that is associated with LLP (Sastry, 1982) and 4) examine the suggestion of Collingridge et al., (1983b) that N-methyl-DL-aspartate preferring amino acid receptors are involved in the induction of LLP. The studies conducted led to the conclusions that 1) LLP is probably generated presynaptically and depression of synaptic responses is localized to the postsynaptic neurone; 2) verapamil appears to antagonize Ca++-dependent depression postsynaptically but it does not block the induction of Ca⁺⁺ dependent LLP; 3) the decrease in excitability of Schaffer collateral terminal regions which correlates with LLP is Ca⁺⁺ dependent but insensitive to verapamil and 4) N-methyl-DL-aspartate preferring receptors are not involved in the induction of LLP.

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