Maurin Y, Enz A, Le Saux F, Besson M J
Brain Res. 1986 Feb 26;366(1-2):379-84. doi: 10.1016/0006-8993(86)91323-5.
In quaking mice (a genetic model of epilepsy with an increased number of noradrenergic neurons) bilateral electrolytic coagulation of locus coeruleus (LC) in adult mice inhibited the convulsions elicited by somatic stimulations while neonatal 6-hydroxydopamine (6-OHDA) treatment remained ineffective upon the convulsions. Biochemical effects of the two treatments differed only in the brainstem where electrolytic lesion decreased while 6-OHDA treatment increased noradrenaline (NA) and 3-methoxy 4-hydroxyphenylethyleneglycol (MHPG) levels. Our results suggest that supernumerary LC neurons mediate the convulsions of the mutants through an action presumably restricted to the brainstem.
在颤抖小鼠(一种癫痫的遗传模型,其中去甲肾上腺素能神经元数量增加)中,成年小鼠双侧蓝斑(LC)电解凝闭可抑制躯体刺激引发的惊厥,而新生小鼠用6-羟基多巴胺(6-OHDA)处理对惊厥无效。两种处理的生化效应仅在脑干有所不同,电解损伤使脑干中去甲肾上腺素(NA)和3-甲氧基4-羟基苯乙二醇(MHPG)水平降低,而6-OHDA处理则使其升高。我们的结果表明,多余的LC神经元可能通过一种可能仅限于脑干的作用来介导突变体的惊厥。