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下丘脑外侧结节核:正常解剖结构及神经疾病中的变化

The hypothalamic lateral tuberal nucleus: normal anatomy and changes in neurological diseases.

作者信息

Kremer H P

机构信息

Department of Neurology, Academic Hospital, Leiden, The Netherlands.

出版信息

Prog Brain Res. 1992;93:249-61. doi: 10.1016/s0079-6123(08)64576-8.

Abstract

The lateral tuberal nucleus is a circumscribed cell mass in the lateral posterior part of the hypothalamus, containing about 60000 neurons. It can be recognized in man and higher primates, probably not in other mammals. Its neurotransmitter content and connections with other parts of the brain are as yet unknown. But receptors for corticotropin-releasing factor and somatostatin, as well as muscarinic cholinergic receptors, benzodiazepine receptors and N-methyl-D-aspartate receptors have been localized within the confines of the nucleus. The lateral tuberal nucleus is affected in a number of human neurodegenerative diseases. Changes in Parkinson's disease are the least obvious: Lewy bodies appear in small amounts, the majority of them apparently lying outside a neuronal perikaryon. Neuronal loss does not occur. In Alzheimer's disease the number of neurons seems to be normal as well. Rarely silver staining tangles occur, and the deposition of A4/beta-protein in amorphous plaques is moderate. Yet, NTL neurons stain heavily in Alz-50 immunocytochemistry, while Alz-50 staining in NTL neurites is very dense. These changes are interpreted as indicating early Alzheimer-related pathology. In Huntington's disease the NTL loses neurons. This loss is related to the severity of the disease: patients who first display motor disturbances at an early age will lose more neurons than those who start later. The relation between these clinical characteristics and the severity of neuronal loss is such, that it seems likely that NTL neurons possess a special vulnerability for the effect of the Huntington gene. This could be related to their NMDA-receptor content. It is hypothesized that the NTL is involved in a neuronal network that regulates feeding and metabolism. NTL pathology may explain the peculiar catabolic state of many patients with Alzheimer's or Huntington's diseases.

摘要

外侧结节核是下丘脑外侧后部一个界限分明的细胞团,包含约60000个神经元。在人类和高等灵长类动物中可以识别出该结构,其他哺乳动物中可能不存在。其神经递质含量以及与大脑其他部位的连接尚不清楚。但促肾上腺皮质激素释放因子和生长抑素的受体,以及毒蕈碱型胆碱能受体、苯二氮䓬受体和N-甲基-D-天冬氨酸受体已定位在该核范围内。外侧结节核在多种人类神经退行性疾病中会受到影响。帕金森病中的变化最不明显:路易小体少量出现,其中大多数显然位于神经元胞体之外。未发生神经元丢失。在阿尔茨海默病中,神经元数量似乎也正常。很少出现银染缠结,A4/β-蛋白在无定形斑块中的沉积程度适中。然而,在Alz-50免疫细胞化学中,外侧结节核神经元染色很深,而外侧结节核神经突中的Alz-50染色非常密集。这些变化被解释为表明与阿尔茨海默病相关的早期病理。在亨廷顿病中,外侧结节核会丢失神经元。这种丢失与疾病的严重程度相关:早年首次出现运动障碍的患者比发病较晚的患者会丢失更多神经元。这些临床特征与神经元丢失严重程度之间的关系表明,外侧结节核神经元似乎对亨廷顿基因的作用具有特殊的易损性。这可能与其NMDA受体含量有关。据推测,外侧结节核参与调节进食和代谢的神经网络。外侧结节核病理可能解释了许多阿尔茨海默病或亨廷顿病患者的特殊分解代谢状态。

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