Abstract
A high-frequency train of electrical stimulation applied to the afferent pathways of the hippocampus produces a long-term potentiation (LTP) of synaptic transmission, which is considered to be a good experimental model of memory processes (Teyler and DiScenna 1987). The mechanisms of the induction and maintenance phases of LTP have been extensively studied in this structure, which plays an important role in memory processes, and the injury of which is known to interfere with learning and memory in humans and animals (Zola-Morgan et al. 1986). There is general agreement that in the CA1 Schaffer collateral associational synapse and the perforant pathway projection to the granule cells of the fascia dentata, the LTP is due to a Ca++ influx produced by the activation of the N-methyl-D-aspartate (NMDA) receptor channel complex (Collingridge and Bliss 1987; Malenka et al. 1989). In contrast, in the mossy fiber synapse, LTP does not involve the NMDA receptor, but is mediated by a rise in [Ca++]i via the activation of voltage-dependent Ca++ channels (Williams and Johnston 1989; Jaffe and Johnston 1990; but see Zalutsky and Nicoll 1990).
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Aniksztejn, L., Ben-Ari, Y. (1991). Blockade of Specific K+ Channels Produces a Ca++ Dependent Form of Long-Term Potentiation in the Hippocampus. In: Ascher, P., Choi, D.W., Christen, Y. (eds) Glutamate, Cell Death and Memory. Research and Perspectives in Neurosciences. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84526-0_6
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DOI: https://doi.org/10.1007/978-3-642-84526-0_6
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