Distinct expressions for synaptic potentiation induced by calcium through voltage-gated calcium and N-methyl-D-aspartate receptor channels in the hippocampal CA1 region

被引:15
作者
Chen, HX [1 ]
Hanse, E [1 ]
Pananceau, M [1 ]
Gustafsson, B [1 ]
机构
[1] Univ Goteborg, Dept Physiol & Pharmacol, S-41390 Gothenburg, Sweden
关键词
hippocampus; synaptic plasticity; long-term potentiation; calcium; voltage-gated calcium channels;
D O I
10.1016/S0306-4522(98)00042-6
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Brief elevation in postsynaptic calcium in hippocampal CAI neurons leads to prolonged changes in synaptic strength. The calcium may enter the postsynaptic neuron via different routes, such as voltage-gated calcium channels or glutamate receptor channels of N-methyl-D-aspartate type, and/or be released from intracellular stores. The manner in which the synapse is altered, leading to the expression of an enhanced/depressed synaptic strength, is still unclear. The present study, performed using whole-cell recording from CA1 pyramidal cells of three- to five-week-old guinea pigs, shows that postsynaptic depolarization alone, allowing for calcium influx through voltage-gated calcium channels, leads to a synaptic potentiation characterized by an altered time-course of the evoked excitatory synaptic response, an unaltered coefficient of variation of that response and a decreased paired-pulse facilitation likely related to a postsynaptic mechanism. These characteristics contrasted with those of long-term potentiation induced via activation of N-methyl-D-aspartate receptor channels, where the time-course was unaltered, the coefficient of variation was decreased and no change in paired-pulse facilitation was observed. Synapses can thus have mechanistically separate, but co-existent, potentiations of synaptic transmission initiated from separate sources for postsynaptic calcium. (C) 1998 IBRO. Published by Elsevier Science Ltd.
引用
收藏
页码:415 / 422
页数:8
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