CHANGES IN BRAIN DOPAMINE AND ACETYLCHOLINE-RELEASE DURING AND FOLLOWING STRESS ARE INDEPENDENT OF THE PITUITARY-ADRENOCORTICAL AXIS

CHANGES IN BRAIN DOPAMINE AND ACETYLCHOLINE-RELEASE DURING AND FOLLOWING STRESS ARE INDEPENDENT OF THE PITUITARY-ADRENOCORTICAL AXIS
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DOI:
10.1016/0006-8993(91)90384-8
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发表时间:
1991-01-04
期刊:
影响因子:
2.9
通讯作者:
ANGELUCCI, L
ANGELUCCI, L
中科院分区:
医学3区
文献类型:
--
作者:
IMPERATO, A;PUGLISIALLEGRA, S;ANGELUCCI, L

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采用微透析技术检测清醒大鼠在120 min束缚应激期间和应激后内侧前额叶皮质、中脑核、尾状核细胞外多巴胺和海马乙酰胆碱的含量。束缚应激迅速刺激内侧前额叶皮层和丘脑核多巴胺的释放和代谢,以及海马乙酰胆碱的释放。50 ~ 60分钟后,尽管大鼠仍然受到抑制,但多巴胺和乙酰胆碱的释放逐渐恢复到基础水平。当动物被释放时,观察到两种神经递质的释放都有相当大的增加。在整个实验中没有观察到纹状体的变化。血浆皮质酮的时间过程并不平行的多巴胺和乙酰胆碱的释放,增加在整个应激过程中,并降低时,动物被释放。肾上腺切除的大鼠对应激和解放的反应与完整大鼠大致相同。外源性皮质酮(0.5-1.5 mg/kg s.c.)没有改变前额叶皮层和丘脑核释放多巴胺和海马释放乙酰胆碱,而刺激它们的3.0毫克/公斤剂量使血浆皮质酮升高到很高的浓度,这在应激期间从未达到过。此外,RU 38486,脑糖皮质激素受体的拮抗剂,没有拮抗应激诱导的神经递质释放的增加。这些结果表明:(1)内侧前额叶皮层和丘脑核的多巴胺释放和海马的乙酰胆碱释放都受到束缚应激和自由应激的刺激,提示这种激活可能是环境突然变化引起的情绪唤醒的神经化学相关;(2)血浆皮质酮的增加与多巴胺和乙酰胆碱释放的增加之间没有因果关系。
Microdialysis was employed to assess extracellular dopamine from medial prefrontal cortex, nucleus accumbens, nucleus caudatus, and acetylcholine from the hippocampus of conscious rats during and after 120 min restraint stress. Restraint stress rapidly stimulated the release and the metabolism of dopamine in the medial prefrontal cortex and in the nucleus accumbens, and acetylcholine release in the hippocampus. Fifty-sixty min later, although rats were still restrained, dopamine and acetylcholine release gradually returned to basal levels. When the animals were freed a considerable increase in the release of both neurotransmitters was observed. No changes in the striatum were observed throughout the experiments. The time-course of plasma corticosterone did not parallel that of dopamine and acetylcholine release, increasing during the whole stress procedure, and decreasing when the animals were released. Adrenalectomized rats responded to stress and liberation in much the same way as intact rats. The administration of exogenous corticosterone (0.5-1.5 mg/kg s.c.) did not change the release of dopamine from the prefrontal cortex and nucleus accumbens, and of acetylcholine from the hippocampus, while the dose of 3.0 mg/kg which stimulated them, raised plasma corticosterone to very high concentrations which had never been attained during stress. Moreover, RU 38486, an antagonist of brain glucocorticoid receptors, did not antagonize the stress-induced increase of neurotransmitter release. These results demonstrate that: (1) dopamine release in the medial prefrontal cortex and nucleus accumbens, and acetylcholine release in the hippocampus are stimulated by restraint stress as well as by freeing the animal, suggesting that such activation may be a neurochemical correlate of emotional arousal produced by sudden environmental changes; (2) there is no cause-effect relationship between increase in plasma corticosterone and increase in dopamine and acetylcholine release.