MODULATION OF LONG-TERM POTENTIATION IN RAT HIPPOCAMPAL PYRAMIDAL NEURONS BY ZINC

被引:71
作者
XIE, XM [1 ]
SMART, TG [1 ]
机构
[1] UNIV LONDON,SCH PHARM,DEPT PHARMACOL,LONDON WC1N 1AX,ENGLAND
来源
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY | 1994年 / 427卷 / 5-6期
基金
英国惠康基金;
关键词
ZINC; LONG-TERM POTENTIATION; EXCITATORY AMINO ACID RECEPTORS; HIPPOCAMPUS; INTRACELLULAR RECORDING; ZINC CHELATOR;
D O I
10.1007/BF00374264
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The phenomenon of long-term potentiation is frequently promulgated as an example of learning and memory mechanisms at the synaptic level in the mammalian central nervous system. In the CA3 region of the hippocampus there is an abundance of zinc, which is located in presynaptic messy fibre nerve terminals. Stimulation of these fibres can cause the release of zinc, which interacts with excitatory amino acid receptors and may therefore modulate long-term potentiation. We now demonstrate in,CA1 and CA3 neurons that zinc (100-300 mu M) enhances non-N-methyl-D-aspartate-receptor-mediated responses whilst reducing excitatory synaptic transmission and inhibiting long-term potentiation. However, by using zinc-chelating agents, endogenously released zinc following high-frequency stimulation in the stratum lucidum does not appear to have any modulatory role in excitatory synaptic transmission and longterm potentiation. These results indicate that an increase in the level of extracellular zinc can limit excitatory synaptic transmission in the CA1 or CA3 region and further suggests that pathologies that can be related to excessive levels of endogenous zinc may have implications for synaptic plasticity in CA3 neurons.
引用
收藏
页码:481 / 486
页数:6
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