Department of Medicine (Neurology) and Center for Health Policy Research and Education, Duke University, Durham, NC (USA) and Department of Veterans' Affairs Medical Center, Durham, NC (USA).
Restor Neurol Neurosci. 1993 Jan 1;5(5):371-6. doi: 10.3233/RNN-1993-55608.
Pharmacologic studies have implicated norepinephrine in amphetamine-facilitated motor recovery following sensorimotor cortex injury in rats. We studied the acute effects of unilateral sensorimotor cortex ablation on the release of norepinephrine in cerebellum with in vivo dialysis. In rats without a cortex lesion, the administration of a single dose of d-amphetamine (2.6 mg/kg base weight, i.p.) resulted in a substantial increase in dialyzable norepinephrine in cerebellum reaching its peak 30-40 min later (∼ 14 pg/μl, not corrected for recovery). The administration of the same dose of d-amphetamine to rats 60 min following a suction-ablation lesion of the right sensorimotor cortex did not result in norepinephrine release into the cerebellar dialysates. These data provide evidence for an acute remote effect of sensorimotor cortex injury on amphetamine-induced norepinephrine release in the cerebellum (diaschisis).
药理学研究表明，去甲肾上腺素在大鼠感觉运动皮层损伤后促进安非他命促进运动功能恢复中起作用。我们通过体内透析研究了单侧感觉运动皮层消融对小脑去甲肾上腺素释放的急性影响。在没有皮层损伤的大鼠中，单次给予安非他命（2.6 毫克/千克基础重量，腹腔注射）导致小脑可透析去甲肾上腺素显著增加，30-40 分钟后达到峰值（约 14 皮克/微升，未校正回收率）。在右侧感觉运动皮层抽吸消融后 60 分钟给予大鼠相同剂量的安非他命，不会导致去甲肾上腺素释放到小脑透析液中。这些数据为感觉运动皮层损伤对安非他命诱导的小脑去甲肾上腺素释放的急性远程影响（传入侧支抑制）提供了证据。
