CORTICOSTRIATAL AND THALAMIC REGULATION OF AMPHETAMINE-INDUCED ASCORBATE RELEASE IN THE NEOSTRIATUM
CORTICOSTRIATAL AND THALAMIC REGULATION OF AMPHETAMINE-INDUCED ASCORBATE RELEASE IN THE NEOSTRIATUM
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DOI：
10.1016/0091-3057(90)90204-u
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发表时间：
1990-01-01
影响因子：
3.6
通讯作者：
REBEC, GV
中科院分区：
文献类型：
--
作者：
BASSETOMUSK, A;REBEC, GV
在大鼠大脑皮层和丘脑腹内侧核（VM）的损害，以研究这些结构的贡献安非他明（AMPH）诱导的抗坏血酸（AA）在新纹状体释放的在体伏安法测量。在至少一周的恢复期后，将大鼠麻醉，并将电化学修饰的碳纤维电极降低到新纹状体中。与假手术和未手术对照组相比，双侧大脑皮质抽吸病变显著降低了AA的基础水平和新纹状体中AMPH释放的AA量。在双侧而非单侧VM丘脑电解损伤后获得了类似的结果。总的来说，这些结果表明，皮质纹状体通路和VM丘脑核参与调节基础和AMPH诱导的AA在新纹状体的释放。
Lesions of cerebral cortex and ventromedial nucleus (VM) of the thalamus were made in rats to investigate the contribution of these structures to amphetamine (AMPH)-induced ascorbate (AA) release in the neostriatum as measured by in vivo voltammetry. Following a recovery period of at least one week, rats were anesthetized, and electrochemically modified, carbon-fiber electrodes were lowered into the neostriatum. Compared to data obtained from sham-operated and unoperated controls, bilateral aspiration lesions of cerebral cortex significantly lowered both the basal level of AA and the amount of AA released by AMPH in the neostriatum. Similar results were obtained after bilateral, but not unilateral electrolytic lesions of the VM thalamus. Collectively, these results suggest that the corticostriatal pathway and the VM thalamic nuclei participate in the regulation of basal and AMPH-induced AA release in the neostriatum.