Fritschi J A, Lauterburg Th, Burgunder J-M
Laboratory of Neuromorphology, Department of Neurology and Department of Clinical Research, University of Bern, Bern, Switzerland.
Neurosci Lett. 2003 Aug 14;347(1):45-8. doi: 10.1016/s0304-3940(03)00616-5.
Rats treated with iminodipropionitrile develop a neurobehaviour syndrome with dyskinesia. Searching for the molecular correlates, we have examined the expression of selected genes involved in neurotransmission in motor regions using hybridization histochemistry. Frontal cortical and thalamic vasoactive intestinal peptide (VIP) expression, and striatal dynorphin, enkephalin (ENK) and substance P expression were increased. No change in cortical cholecystokinin (CCK), ENK, glutamic acid decarboxylase (GAD) and somatostatin (SRIF) expression, in striatal GAD, SRIF, nitric oxide synthase (NOS) and guanylate cyclase expression, and in thalamic CCK, GAD and thyrotropin-releasing hormone expression was found. NOS expression in the subthalamic nucleus as well as tyrosine hydroxylase, GAD and CCK expression in the substantia nigra were unchanged. These results confirm the involvement of striatal projection neurons in dyskinesia and suggest a novel role for VIP.
用亚氨基二丙腈处理的大鼠会出现伴有运动障碍的神经行为综合征。为了寻找分子关联,我们使用杂交组织化学研究了运动区域中参与神经传递的特定基因的表达。额叶皮质和丘脑血管活性肠肽(VIP)表达以及纹状体强啡肽、脑啡肽(ENK)和P物质表达增加。未发现皮质胆囊收缩素(CCK)、ENK、谷氨酸脱羧酶(GAD)和生长抑素(SRIF)表达、纹状体GAD、SRIF、一氧化氮合酶(NOS)和鸟苷酸环化酶表达以及丘脑CCK、GAD和促甲状腺激素释放激素表达有变化。丘脑底核中的NOS表达以及黑质中的酪氨酸羟化酶、GAD和CCK表达未改变。这些结果证实了纹状体投射神经元参与运动障碍,并提示了VIP的新作用。