首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Postsynaptic factors in the expression of long-term potentiation (LTP): increased glutamate receptor binding following LTP induction in vivo.
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Postsynaptic factors in the expression of long-term potentiation (LTP): increased glutamate receptor binding following LTP induction in vivo.

机译:突触后因子在长期增强(LTP)中的表达:体内LTP诱导后增加的谷氨酸受体结合。

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摘要

Several lines of evidence indicate that LTP in the hippocampus is associated with a change in the properties of postsynaptic glutamate receptors. In the present study, we used quantitative autoradiography to examine the binding properties of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) and N-methyl-D-aspartate subclasses of glutamate receptors in frozen brain sections obtained from rats in which perforant-path LTP was induced in vivo. Induction of LTP resulted in a selective increase in [3H]AMPA binding in those hippocampal subfields receiving perforant-path axons. Increases in [3H]AMPA binding in dentate gyrus (stratum moleculare) were highly correlated with the magnitude of LTP recorded in this structure. Scatchard analyses of [3H]AMPA and 6-cyano-7-nitro-[3H]quinoxaline-2,3-dione (an AMPA receptor antagonist) binding in the dentate gyrus indicated that LTP induction resulted in an increase in the number of AMPA receptor binding sites. No changes in the binding of 3H-labeled N-[1-(thienyl)cyclohexyl]piperidine (an N-methyl-D-aspartate receptor antagonist) were observed in any hippocampal subfield. These results suggest that a modification in postsynaptic AMPA receptors plays a role in the expression of synaptic enhancement following LTP induction in the hippocampus.
机译:几条证据表明,海马中的LTP与突触后谷氨酸受体特性的变化有关。在本研究中,我们使用定量放射自显影技术检查冷冻状态下谷氨酸受体的α-氨基-3-羟基-5-甲基-4-异恶唑丙酸酯(AMPA)和N-甲基-D-天冬氨酸亚类的结合特性从大鼠体内获得的脑切片,其中在体内诱导了穿孔路径LTP。 LTP的诱导导致在那些接受穿孔路径轴突的海马亚区中[3H] AMPA结合的选择性增加。齿状回(层状分子)中[3H] AMPA结合的增加与该结构中记录的LTP的量高度相关。对齿状回中的[3H] AMPA和6-氰基-7-硝基-[3H]喹喔啉-2,3-二酮(一种AMPA受体拮抗剂)结合的Scatchard分析表明,LTP诱导导致AMPA数量增加受体结合位点。在任何海马亚区均未观察到3H标记的N- [1-(噻吩基)环己基]哌啶(N-甲基-D-天冬氨酸受体拮抗剂)的结合变化。这些结果表明,在海马中LTP诱导后,突触后AMPA受体的修饰在突触增强的表达中起作用。

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