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在边缘皮层中,突触可塑性和识别记忆的机制。

Mechanisms of synaptic plasticity and recognition memory in the perirhinal cortex.

机构信息

School of Physiology and Pharmacology, University of Bristol, Bristol, United Kingdom.

出版信息

Prog Mol Biol Transl Sci. 2014;122:193-209. doi: 10.1016/B978-0-12-420170-5.00007-6.

Abstract

Learning is widely believed to involve synaptic plasticity, employing mechanisms such as those used in long-term potentiation (LTP) and long-term depression (LTD). In this chapter, we will review work on mechanisms of synaptic plasticity in perirhinal cortex in vitro and relate these findings to studies underlying recognition memory in vivo. We describe how antagonism of different glutamate and acetylcholine receptors, inhibition of nitric oxide synthase, inhibition of CREB phosphorylation, and interfering with glutamate AMPA receptor internalization can produce deficits in synaptic plasticity in vitro. Inhibition of each of these different mechanisms in vivo also results in recognition memory deficits. Therefore, we provide strong evidence that synaptic plastic mechanisms are necessary for the information processing and storage that underlies object recognition memory.

摘要

学习被广泛认为涉及突触可塑性,采用的机制如长时程增强(LTP)和长时程抑制(LTD)。在这一章中,我们将回顾在体外海人酸诱导的颞叶皮层突触可塑性机制的研究工作,并将这些发现与体内的识别记忆研究联系起来。我们描述了拮抗不同的谷氨酸和乙酰胆碱受体、抑制一氧化氮合酶、抑制 CREB 磷酸化以及干扰谷氨酸 AMPA 受体内化如何在体外产生突触可塑性缺陷。在体内抑制这些不同机制中的每一种也会导致识别记忆缺陷。因此,我们提供了强有力的证据表明,突触可塑性机制是物体识别记忆信息处理和存储的必要条件。

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