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通过对丘脑皮质回路的建模研究表明,视觉诱导的 LTP 会改变人类视觉皮层的层间连接。

Modelling thalamocortical circuitry shows that visually induced LTP changes laminar connectivity in human visual cortex.

机构信息

School of Pharmacy, University of Auckland, Auckland, New Zealand.

Centre for Psychedelic Research, Department of Medicine, Imperial College London, London, United Kingdom.

出版信息

PLoS Comput Biol. 2021 Jan 21;17(1):e1008414. doi: 10.1371/journal.pcbi.1008414. eCollection 2021 Jan.

DOI:10.1371/journal.pcbi.1008414
PMID:33476341
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7853500/
Abstract

Neuroplasticity is essential to learning and memory in the brain; it has therefore also been implicated in numerous neurological and psychiatric disorders, making measuring the state of neuroplasticity of foremost importance to clinical neuroscience. Long-term potentiation (LTP) is a key mechanism of neuroplasticity and has been studied extensively, and invasively in non-human animals. Translation to human application largely relies on the validation of non-invasive measures of LTP. The current study presents a generative thalamocortical computational model of visual cortex for investigating and replicating interlaminar connectivity changes using non-invasive EEG recording of humans. The model is combined with a commonly used visual sensory LTP paradigm and fit to the empirical EEG data using dynamic causal modelling. The thalamocortical model demonstrated remarkable accuracy recapitulating post-tetanus changes seen in invasive research, including increased excitatory connectivity from thalamus to layer IV and from layer IV to II/III, established major sites of LTP in visual cortex. These findings provide justification for the implementation of the presented thalamocortical model for ERP research, including to provide increased detail on the nature of changes that underlie LTP induced in visual cortex. Future applications include translating rodent findings to non-invasive research in humans concerning deficits to LTP that may underlie neurological and psychiatric disease.

摘要

神经可塑性对于大脑的学习和记忆至关重要;因此,它也与许多神经和精神疾病有关,这使得测量神经可塑性状态成为临床神经科学的首要任务。长时程增强(LTP)是神经可塑性的关键机制,已经在非人类动物中进行了广泛的研究,包括侵入性研究。向人类应用的转化在很大程度上依赖于对 LTP 的非侵入性测量的验证。本研究提出了一个视觉皮层的丘脑皮质生成计算模型,用于使用人类的非侵入性 EEG 记录来研究和复制层间连接变化。该模型与常用的视觉感觉 LTP 范式相结合,并使用因果建模对经验 EEG 数据进行拟合。该丘脑皮质模型对侵入性研究中所见的强直后变化具有显著的准确性,包括从丘脑到第四层和从第四层到 II/III 层的兴奋性连接增加,确定了视觉皮层中 LTP 的主要部位。这些发现为实施所提出的丘脑皮质模型进行 ERP 研究提供了依据,包括提供关于视觉皮层中 LTP 诱导的变化性质的更多细节。未来的应用包括将啮齿动物的研究结果转化为关于神经和精神疾病中 LTP 缺陷的非侵入性人类研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/a21b95b79bc9/pcbi.1008414.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/39d238b4f40b/pcbi.1008414.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/92cb5aea1107/pcbi.1008414.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/fac03be186fc/pcbi.1008414.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/c1d2b36f6dcf/pcbi.1008414.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/56246b50b1d1/pcbi.1008414.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/49630d215d7f/pcbi.1008414.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/a21b95b79bc9/pcbi.1008414.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/39d238b4f40b/pcbi.1008414.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/92cb5aea1107/pcbi.1008414.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/fac03be186fc/pcbi.1008414.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/c1d2b36f6dcf/pcbi.1008414.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/56246b50b1d1/pcbi.1008414.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/49630d215d7f/pcbi.1008414.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6749/7853500/a21b95b79bc9/pcbi.1008414.g007.jpg

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