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围产期吗啡II:皮质可塑性的变化

Perinatal morphine II: changes in cortical plasticity.

作者信息

Germani E, Lesma E, De Biasi S, Di Giulio A M, Bertelli A, Gorio A

机构信息

Department of Medical Pharmacology, University of Milan, Italy.

出版信息

J Neurosci Res. 1995 Dec 15;42(6):829-34. doi: 10.1002/jnr.490420611.

Abstract

We have previously shown that perinatal exposure to morphine impairs reactive plasticity of serotonin (5-HT) neurons following selective neonatal lesion (Gorio et al., J Neurosci Res 34:462-471, 1993). This study shows that morphine inhibits also that the compensatory sprouting of intact axons after partial denervation. Neonatal 6-OHDA injection causes norepinephrine (NE) depletion in the frontal cortex, which triggers a compensatory increase of dopamine, serotonin (5-HT), and met-enkephalin content correlated by the increased density of tyrosine hydroxylase- and 5-HT-positive axons. In perinatal morphine-treated rats, no compensatory changes are observed after neonatal 6-OHDA depletion of NE in the frontal cortex.

摘要

我们之前已经表明,围产期暴露于吗啡会损害选择性新生损伤后5-羟色胺(5-HT)神经元的反应性可塑性(Gorio等人,《神经科学研究杂志》34:462 - 471,1993年)。本研究表明,吗啡还会抑制部分去神经后完整轴突的代偿性发芽。新生大鼠注射6-羟基多巴胺会导致额叶皮质去甲肾上腺素(NE)耗竭,进而引发多巴胺、5-羟色胺(5-HT)和甲硫氨酸脑啡肽含量的代偿性增加,这与酪氨酸羟化酶和5-HT阳性轴突密度增加相关。在围产期经吗啡处理的大鼠中,额叶皮质NE经新生期6-羟基多巴胺耗竭后未观察到代偿性变化。

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