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丘脑前部病变会阻止压后皮质切片中的突触可塑性:扩展间脑失忆症的病理学范围。

Anterior thalamic lesions stop synaptic plasticity in retrosplenial cortex slices: expanding the pathology of diencephalic amnesia.

作者信息

Garden Derek L F, Massey Peter V, Caruana Douglas A, Johnson Ben, Warburton E Clea, Aggleton John P, Bashir Zafar I

机构信息

MRC Centre for Synaptic Plasticity, Department of Anatomy, University of Bristol, Bristol BS8 1TD, UK.

出版信息

Brain. 2009 Jul;132(Pt 7):1847-57. doi: 10.1093/brain/awp090. Epub 2009 Apr 29.

DOI:10.1093/brain/awp090
PMID:19403787
Abstract

Recent, convergent evidence places the anterior thalamic nuclei at the heart of diencephalic amnesia. However, the reasons for the severe memory loss in diencephalic amnesia remain unknown. A potential clue comes from the dense, reciprocal connections between the anterior thalamic nuclei and retrosplenial cortex, another region vital for memory. We now report a loss of synaptic plasticity [long-term depression (LTD)] in rat retrosplenial cortex slices months following an anterior thalamic lesion. The loss of LTD was lamina-specific, occurring only in superficial layers of the cortex and was associated with a decrease in GABA(A)-mediated inhibitory transmission. As retrosplenial cortex is itself vital for memory, this distal lesion effect will amplify the impact of anterior thalamic lesions. These findings not only provide novel insights into the functional pathology of diencephalic amnesia and have implications for the aetiology of the posterior cingulate hypoactivity in Alzheimer's disease, but also show how distal changes in plasticity could contribute to diaschisis.

摘要

近期,多项相互印证的证据表明丘脑前核是间脑性遗忘症的核心所在。然而,间脑性遗忘症中严重记忆丧失的原因仍不明确。一个潜在的线索来自丘脑前核与压后皮质之间密集的相互连接,压后皮质是另一个对记忆至关重要的区域。我们现在报告,在丘脑前核损伤数月后,大鼠压后皮质切片中出现了突触可塑性[长时程抑制(LTD)]丧失。LTD的丧失具有层特异性,仅发生在皮质的浅层,并且与GABA(A)介导的抑制性传递减少有关。由于压后皮质本身对记忆至关重要,这种远距离损伤效应将放大丘脑前核损伤的影响。这些发现不仅为间脑性遗忘症的功能病理学提供了新的见解,并对阿尔茨海默病中后扣带回活动减退的病因学具有启示意义,还展示了可塑性的远距离变化如何导致神经机能联系障碍。

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