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出生后早期暴露于酒精的大鼠锥体神经元中树突棘密度降低。

Reduced density of dendritic spines in pyramidal neurons of rats exposed to alcohol during early postnatal life.

作者信息

De Giorgio Andrea, Granato Alberto

机构信息

Department of Psychology, Catholic University, Largo A. Gemelli 1, 20123 Milan, Italy.

出版信息

Int J Dev Neurosci. 2015 Apr;41:74-9. doi: 10.1016/j.ijdevneu.2015.01.005. Epub 2015 Jan 30.

Abstract

Dendritic spines are the main postsynaptic sites of excitatory connections of neocortical pyramidal neurons. Alterations of spine shape, number, and density can be observed in different mental diseases, including those caused by developmental alcohol exposure. Pyramidal neurons of layer 2/3 are the most abundant cells of the neocortex and represent the main source of associative cortico-cortical connections. These neurons are essential for higher functions mediated by the cortex such as feature selection and perceptual grouping. Furthermore, their connections have been shown to be altered in experimental models of fetal alcohol spectrum disorders. Here, we used a Golgi-like tracing method to study the spine density of layer 2/3 associative pyramidal neurons in the somatosensory cortex of adult rats exposed to alcohol during the first postnatal week. The main result of the present study is represented by the decreased spine density in the apical dendrite of alcohol-treated rats, as compared to controls. As to the basal dendritic tree, there were no significant differences between the experimental and the control group. A decreased density of dendritic spines in the apical dendrite may impair the excitatory input onto pyramidal neurons, thus resulting in a widespread alteration of the cortical information flow.

摘要

树突棘是新皮质锥体细胞兴奋性连接的主要突触后位点。在不同的精神疾病中,包括由发育过程中酒精暴露引起的疾病,均可观察到树突棘形状、数量和密度的改变。2/3层的锥体细胞是新皮质中数量最多的细胞,是联合皮质-皮质连接的主要来源。这些神经元对于由皮质介导的高级功能,如特征选择和知觉分组,至关重要。此外,在胎儿酒精谱系障碍的实验模型中,已证明它们的连接发生了改变。在此,我们使用一种类似高尔基染色的追踪方法,来研究在出生后第一周暴露于酒精的成年大鼠体感皮质中,2/3层联合锥体细胞的树突棘密度。本研究的主要结果是,与对照组相比,酒精处理大鼠的顶端树突中树突棘密度降低。至于基底树突,实验组和对照组之间没有显著差异。顶端树突中树突棘密度降低可能会损害锥体细胞上的兴奋性输入,从而导致皮质信息流的广泛改变。

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