Melamed E, Pikarski E, Goldberg A, Rosenthal J, Uzzan A, Conforti N
Brain Res. 1986 Dec 3;399(1):178-80. doi: 10.1016/0006-8993(86)90615-3.
In mice, prior destruction of striatal 5-hydroxytryptamine (5-HT) neurons by intrastriatal or intraventricular injections of 5,7-dihydroxytryptamine did not abolish or attenuate DA depletions produced in striatum by 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP). This suggests that although they contain monoamine oxidase type B, the oxidative conversion of MPTP to 1-methyl-4-phenyl-pyridinium ion (MPP+) does not take place in 5-HT neurons. Likewise, decortication and kainic acid lesions did not prevent or enhance striatal MPTP-induced DA decrements suggesting that corticostriatal projections and striatal neurons are not involved in the mechanisms of MPTP neurotoxicity.
在小鼠中，通过纹状体内或脑室内注射5,7 - 二羟基色胺预先破坏纹状体5 - 羟色胺（5 - HT）神经元，并不会消除或减弱1 - 甲基 - 4 - 苯基 - 1,2,5,6 - 四氢吡啶（MPTP）在纹状体中引起的多巴胺（DA）耗竭。这表明，尽管5 - HT神经元含有B型单胺氧化酶，但MPTP向1 - 甲基 - 4 - 苯基吡啶离子（MPP +）的氧化转化并不在5 - HT神经元中发生。同样，去皮质和 kainic 酸损伤并不会预防或增强纹状体MPTP诱导的DA减少，这表明皮质纹状体投射和纹状体神经元不参与MPTP神经毒性机制。
