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非人灵长类动物的新皮质梗死会导致Meynert基底核中胆碱能神经元的形态损伤受限。

Neocortical infarction in subhuman primates leads to restricted morphological damage of the cholinergic neurons in the nucleus basalis of Meynert.

作者信息

Liberini P, Pioro E P, Maysinger D, Cuello A C

机构信息

Department of Pharmacology and Therapeutics, McGill University, Montreal, Que., Canada.

出版信息

Brain Res. 1994 Jun 13;648(1):1-8. doi: 10.1016/0006-8993(94)91897-x.

DOI:10.1016/0006-8993(94)91897-x
PMID:7922512
Abstract

The aim of the present study was to investigate the long-term effect of cortical infarction on the subhuman primate (Cercopithecus aethiops) basal forebrain. The lesion, carried out by cauterizing the pial blood vessels supplying the left fronto-parieto-temporal neocortex, induced retrograde degenerative processes within the ipsilateral nucleus basalis of Meynert. The morphometrical analysis revealed that significant shrinkage of cholinergic neurons and loss of neuritic processes were localized within the intermediate regions of the nucleus basalis. The average cross-sectional areas of choline acetyltransferase-immunoreactive neurons in the intermedio-ventral (Ch4iv) and intermedio-dorsal (Ch4id) nucleus basalis were decreased to 62.5 +/- 9.5 and 58.0 +/- 8.6%, respectively, of the sham-operated values. Although an apparent loss of Nissl-stained magnocellular neurons in Ch4iv and Ch4id was found by applying a quantitative analysis based on a perikaryal-size criterion, data obtained by the quantification of immunostained material failed to reveal any significant decrease of cholinergic cell density. Results are discussed in view of future application of this ischemic model to study processes of retrograde degeneration following cortical target removal and to assess potential neurotrophic and neuroprotective properties of pharmacologic agents.

摘要

本研究的目的是调查皮质梗死对非人灵长类动物(埃塞俄比亚猕猴)基底前脑的长期影响。通过烧灼供应左侧额顶颞新皮质的软脑膜血管造成损伤,诱发同侧Meynert基底核内的逆行性变性过程。形态学分析显示,胆碱能神经元的显著萎缩和神经突的丧失定位于基底核的中间区域。中间腹侧(Ch4iv)和中间背侧(Ch4id)基底核中胆碱乙酰转移酶免疫反应性神经元的平均横截面积分别降至假手术值的62.5±9.5%和58.0±8.6%。尽管通过基于胞体大小标准的定量分析发现Ch4iv和Ch4id中尼氏染色的大细胞神经元明显丧失,但通过免疫染色材料定量获得的数据未能显示胆碱能细胞密度有任何显著降低。鉴于该缺血模型未来在研究皮质靶点切除后的逆行性变性过程以及评估药物潜在的神经营养和神经保护特性方面的应用,对结果进行了讨论。

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Memory impairment in aged primates is associated with focal death of cortical neurons and atrophy of subcortical neurons.老年灵长类动物的记忆障碍与皮质神经元的局灶性死亡和皮质下神经元的萎缩有关。
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Cholinergic changes in the APP23 transgenic mouse model of cerebral amyloidosis.
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Experimental neurotrophic factor therapy leads to cortical synaptic remodeling and compensates for behavioral deficits.实验性神经营养因子疗法可导致皮质突触重塑并弥补行为缺陷。
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