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多巴胺耗竭对大鼠伏隔核壳部和核心部中等棘状神经元形态的影响。

Effects of dopamine depletion on the morphology of medium spiny neurons in the shell and core of the rat nucleus accumbens.

作者信息

Meredith G E, Ypma P, Zahm D S

机构信息

Department of Anatomy and Embryology, Faculty of Medicine, Vrije University, Amsterdam, The Netherlands.

出版信息

J Neurosci. 1995 May;15(5 Pt 2):3808-20. doi: 10.1523/JNEUROSCI.15-05-03808.1995.

Abstract

Nucleus accumbens receives a dense dopaminergic innervation which is important in regulating motivated states of behavior such as goal-directed actions, stimulus-reward associations and reinforcement of addictive substances. The shell and core territories of this nucleus each receive functionally and morphologically distinct dopaminergic inputs and lesions of the ascending pathways totally deprive the core but not the shell of dopaminergic fibers. Medium spiny neurons are the principal targets of dopaminergic terminals. The present study explored whether the loss of dopamine inputs can affect these neurons and whether cells in the shell and core would be equally susceptible to such a loss. Intracellular injection in fixed slices and neuronal reconstruction were used to analyze the dendritic trees of 62 neurons in the shell and core of animals that received a unilateral, chronic 6-hydroxydopamine lesion of the medial forebrain bundle. In the dopamine-depleted core, dendrites are significantly shorter (16% decrease) than in the intact core and in both the dopamine-depleted core and lateral shell, dendrites are less spiny than in respective control regions. Dopamine loss in the medial shell is associated with significantly more tortuous dendrites that are lower in spine density. However, the number of spines is not reduced which may mean that the increase recorded for segment length, although insignificant in tests, could be responsible for the change in spine density. These data suggest that the loss of dopamine can affect accumbal neuronal morphology and, moreover, can affect neuronal structures differentially in the shell and core.

摘要

伏隔核接受密集的多巴胺能神经支配,这在调节行为的动机状态中很重要,如目标导向行为、刺激-奖励关联以及成瘾物质的强化作用。该核的壳区和核心区分别接受功能和形态上不同的多巴胺能输入,上行通路的损伤完全剥夺了核心区而非壳区的多巴胺能纤维。中等棘状神经元是多巴胺能终末的主要靶点。本研究探讨了多巴胺输入的丧失是否会影响这些神经元,以及壳区和核心区的细胞对这种丧失是否同样敏感。在固定切片中进行细胞内注射和神经元重建,以分析接受内侧前脑束单侧慢性6-羟基多巴胺损伤的动物的壳区和核心区中62个神经元的树突树。在多巴胺耗竭的核心区,树突明显比完整核心区短(减少16%),并且在多巴胺耗竭的核心区和外侧壳区,树突的棘突都比各自的对照区域少。内侧壳区的多巴胺丧失与明显更曲折且棘突密度更低的树突有关。然而,棘突的数量并未减少,这可能意味着尽管在测试中不显著,但记录到的节段长度增加可能是棘突密度变化的原因。这些数据表明,多巴胺的丧失会影响伏隔核神经元的形态,而且会在壳区和核心区对神经元结构产生不同的影响。

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