Jackson-Lewis V, Vila M, Djaldetti R, Guegan C, Liberatore G, Liu J, O'Malley K L, Burke R E, Przedborski S
Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York 10032, USA.
J Comp Neurol. 2000 Aug 28;424(3):476-88. doi: 10.1002/1096-9861(20000828)424:3<476::aid-cne6>3.0.co;2-0.
Dopaminergic neurons in the substantia nigra pars compacta (SNpc) undergo natural cell death during development in rats. Controversy exists as to the occurrence of this phenomenon in SNpc dopaminergic neurons in the developing mouse. Herein, by using an array of morphologic techniques, we show that many SNpc neurons fulfill the criteria for apoptosis and that the number of apoptotic neurons in the SNpc vary in a time-dependent manner from postnatal day 2 to 32. These dying neurons also show evidence of DNA fragmentation, of activated caspase-3, and of cleavage of beta-actin. Some, but not all of the SNpc apoptotic neurons still express their phenotypic marker tyrosine hydroxylase, confirming their dopaminergic nature. Consistent with the importance of target-derived trophic support in modulating developmental cell death, we demonstrate that destruction of intrinsic striatal neurons by a local injection of quinolinic acid (QA) dramatically enhances the magnitude of SNpc apoptosis and results in a lower number of adult SNpc dopaminergic neurons. Strengthening the apoptotic nature of the observed SNpc developmental cell death, we demonstrate that overexpression of the anti-apoptotic protein Bcl-2 attenuates both natural and QA-induced SNpc apoptosis. The present study provides compelling evidence that developmental neuronal death with a morphology of apoptosis does occur in the SNpc of mice and that this process plays a critical role in regulating the adult number of dopaminergic neurons in the SNpc.
大鼠黑质致密部(SNpc)中的多巴胺能神经元在发育过程中会发生自然细胞死亡。关于这种现象在发育中小鼠的SNpc多巴胺能神经元中是否存在存在争议。在此,通过使用一系列形态学技术,我们表明许多SNpc神经元符合凋亡标准,并且从出生后第2天到32天,SNpc中凋亡神经元的数量呈时间依赖性变化。这些正在死亡的神经元还表现出DNA片段化、半胱天冬酶-3激活以及β-肌动蛋白裂解的证据。一些(但不是全部)SNpc凋亡神经元仍表达其表型标志物酪氨酸羟化酶,证实了它们的多巴胺能性质。与靶源性营养支持在调节发育性细胞死亡中的重要性一致,我们证明通过局部注射喹啉酸(QA)破坏纹状体内在神经元会显著增强SNpc凋亡的程度,并导致成年SNpc多巴胺能神经元数量减少。为了强化所观察到的SNpc发育性细胞死亡的凋亡性质,我们证明抗凋亡蛋白Bcl-2的过表达会减弱自然和QA诱导的SNpc凋亡。本研究提供了令人信服的证据,表明具有凋亡形态的发育性神经元死亡确实发生在小鼠的SNpc中,并且这一过程在调节成年SNpc中多巴胺能神经元的数量方面起着关键作用。