Saji M, Blau A D, Volpe B T
Department of Neurobiology, Faculty of Life Sciences, Tottori School of Medicine, Yonago Shi, Japan.
Exp Neurol. 1996 Sep;141(1):120-9. doi: 10.1006/exnr.1996.0145.
Transneuronal degeneration (TND) of neurons in the substantia nigra reticulata (SNR) occurs after initial ischemic or neurotoxin damage to the striatum. The mechanism is incompletely understood. In rats ibotenic acid (IBO) lesion of the caudate nucleus (CN) and the globus pallidus (GP) caused, 3 weeks later, a 47% loss of neurons (P < 0.001) in the SNR. Rats with IBO lesion confined to either the CN or the GP had SNR neuron numbers comparable to control. The volume of the SNR was decreased, as expected, in all groups with striatal lesions. To test whether the subthalamic nucleus (STN) played a role in the demise of SNR neurons, the STN was lesioned 1 week before animals were exposed to CN and GP injury. STN ablation prevented the expected SNR neuron loss. Based on the current information about basal ganglia anatomy, an imbalance between GABAergic and glutamatergic afferents may have caused TND in the SNR. These results suggest that the potential for the release of intrinsic excitotoxicity exists within certain anatomic networks.
黑质网状部（SNR）神经元的跨神经元变性（TND）发生在纹状体最初遭受缺血或神经毒素损伤之后。其机制尚未完全明确。在大鼠中，尾状核（CN）和苍白球（GP）的鹅膏蕈氨酸（IBO）损伤在3周后导致SNR中47%的神经元丢失（P < 0.001）。仅CN或GP受到IBO损伤的大鼠，其SNR神经元数量与对照组相当。正如预期的那样，所有纹状体损伤组的SNR体积均减小。为了测试丘脑底核（STN）是否在SNR神经元死亡中起作用，在动物遭受CN和GP损伤前1周对STN进行损伤。STN切除可防止预期的SNR神经元丢失。基于目前关于基底神经节解剖结构的信息，GABA能和谷氨酸能传入之间的失衡可能导致了SNR中的TND。这些结果表明，在某些解剖网络中存在释放内源性兴奋性毒性的可能性。
