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海马体长期抑郁的突触后诱导与突触前表达

Postsynaptic induction and presynaptic expression of hippocampal long-term depression.

作者信息

Bolshakov V Y, Siegelbaum S A

机构信息

Department of Pharmacology, Howard Hughes Medical Institute, Columbia University, New York, NY 10032.

出版信息

Science. 1994 May 20;264(5162):1148-52. doi: 10.1126/science.7909958.

DOI:10.1126/science.7909958
PMID:7909958
Abstract

Long-term depression (LTD) is an activity-dependent decrease in synaptic efficacy that together with its counterpart, long-term potentiation, is thought to be an important cellular mechanism for learning and memory in the mammalian brain. The induction of LTD in hippocampal CA1 pyramidal neurons in neonatal rats is shown to depend on postsynaptic calcium ion entry through L-type voltage-gated calcium channels paired with the activation of metabotropic glutamate receptors. Although induced postsynaptically, LTD is due to a long-term decrease in transmitter release from presynaptic terminals. This suggests that LTD is likely to require the production of a retrograde messenger.

摘要

长时程抑制(LTD)是一种依赖于活动的突触效能降低现象,它与其对应物长时程增强一起,被认为是哺乳动物大脑学习和记忆的重要细胞机制。新生大鼠海马CA1锥体神经元中LTD的诱导依赖于突触后钙离子通过L型电压门控钙通道内流,并与代谢型谷氨酸受体的激活相偶联。尽管LTD是突触后诱导产生的,但其原因是突触前终末递质释放的长期减少。这表明LTD可能需要产生一种逆行信使。

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