MONOAMINE NEUROTRANSMITTER METABOLISM IN MICROENCEPHALIC RAT-BRAIN AFTER PRENATAL METHYLAZOXYMETHANOL TREATMENT
MONOAMINE NEUROTRANSMITTER METABOLISM IN MICROENCEPHALIC RAT-BRAIN AFTER PRENATAL METHYLAZOXYMETHANOL TREATMENT
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DOI：
10.1016/0361-9230(84)90088-1
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发表时间：
1984-01-01
影响因子：
3.8
通讯作者：
JONSSON, G
中科院分区：
文献类型：
--
作者：
HALLMAN, H;JONSSON, G
在胎儿阶段给予甲基偶氮氧甲醇（MAM）可导致前脑小脑畸形，大脑皮质、纹状体和海马严重萎缩。内源性单胺的浓度显着增加萎缩区，而总量基本不变。MAM处理动物的纹状体多巴胺和皮质去甲肾上腺素[去甲肾上腺素]神经末梢在蔗糖密度梯度中显示出未改变的沉降特性，估计具有正常的递质水平。γ-丁内酯诱导多巴胺水平的增加，其抵消阿扑吗啡后MAM基本上没有改变。萎缩区的单胺神经终末野发育至正常大小，导致神经支配过度。进行单胺代谢物水平分析、单胺氧化酶抑制后单胺增加和酪氨酸羟化酶抑制后儿茶酚酶消失，以获得单胺周转率信息。有一个基本上不变，或一个小的减少，单胺营业额在萎缩的地区时，计算每单胺神经末梢，增加时，计算每单位重量的组织。
Administration of methylazoxymethanol (MAM) in the fetal stage leads to forebrain microencephaly with a severe atrophy in cerebral cortex, striatum and hippocampus. The concentration of endogenous monoamines was markedly increased in the atrophic regions while total amount was largely unchanged. Striatal dopamine and cortical noradrenaline [norepinephrine] nerve terminals from MAM treated animals showed unaltered sedimentation properties in a sucrose density gradient and were estimated to have normal transmitter levels. .gamma.-Butyrolactone induced increase in dopamine levels and its counteraction by apomorphine was essentially unaltered after MAM. The monoamine nerve terminal fields develop to their normal size in the atrophic regions leading to a hyperinnervation. Analysis of monoamine metabolite levels, increase of monoamines after monoamine oxidase inhibition, and disappearance of catecholamies after tyrosine hydroxylase inhibition were conducted to obtain information on monoamine turnover. There was an essentially unaltered, or a small reduction of, monoamine turnover in the atrophic regions when calculated per monoamine nerve terminal, which increased when calculated per unit weight of the tissue.