Hallman H, Jonsson G
Brain Res Bull. 1984 Sep;13(3):383-9. doi: 10.1016/0361-9230(84)90088-1.
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 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. These data give further support for the view that 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 catecholamines after tyrosine hydroxylase inhibition were conducted to obtain information on monoamine turnover. The results indicated an essentially unaltered, or a small reduction of, monoamine turnover in the atrophic regions when calculated per monoamine nerve terminal, while increased when calculated per unit weight of the tissue.
在胎儿期给予甲基偶氮甲醇（MAM）会导致前脑小头畸形，大脑皮层、纹状体和海马体出现严重萎缩。萎缩区域内源性单胺的浓度显著增加，而总量基本不变。来自MAM处理动物的纹状体多巴胺和皮层去甲肾上腺素神经末梢在蔗糖密度梯度中的沉降特性未改变，且估计其递质水平正常。MAM处理后，γ-丁内酯诱导的多巴胺水平升高及其被阿扑吗啡的拮抗作用基本未改变。这些数据进一步支持了这样一种观点，即单胺神经末梢场在萎缩区域发育至正常大小，导致神经支配过度。为了获取有关单胺周转的信息，对单胺代谢物水平、单胺氧化酶抑制后单胺的增加以及酪氨酸羟化酶抑制后儿茶酚胺的消失进行了分析。结果表明，按每个单胺神经末梢计算，萎缩区域的单胺周转基本未改变或略有降低，而按组织单位重量计算则增加。
