α-去甲肾上腺素能激动剂和拮抗剂影响大鼠感觉运动皮层切除后恢复和保持走梁能力。

α-Noradrenergic agonists and antagonists affect recovery and maintenance of beam-walking ability after sensorimotor cortex ablation in the rat.

机构信息

Departments of Psychology and Physiology, The University of New Mexico, Albuquerque, NM 87131 (U.S.A.).

出版信息

Restor Neurol Neurosci. 1992 Jan 1;4(1):1-11. doi: 10.3233/RNN-1992-4101.

DOI:10.3233/RNN-1992-4101

Abstract

Rats trained to traverse a narrow elevated beam were given a single intraperitoneal injection of either D-amphetamine, clonidine, L-phenylephrine, prazosin, yohimbine, or saline 24 h after ablation of the right sensorimotor cortex and tested for recovery of beam-walking (BW) ability to day 16 postsurgery. Clonidine, prazosin and L-phenylephrine did not significantly affect BW recovery. A 10 mg/kg dose of yohimbine significantly accelerated BW recovery, as did D-amphetamine (2 mg/kg). Since D-amphetamine and yohimbine both increase norepinephrine (NE) release and prior research has implicated NE but not dopamine in BW recovery, these data support the hypothesis that increased NE release benefits functional recovery in this model of cortical injury. However, a possible role of dopaminergic or serotonergic influences of D-amphetamine or yohimbine treatment cannot be ruled out. To investigate the role of the NE system in maintenance of recovery, animals recovered from BW deficits 18 days after injury were administered clonidine, prazosin, or yohimbine and retested on the BW task. Both the α1-NE antagonist prazosin (2 or 4 mg/kg) and the α2-NE agonist clonidine (0.1 or 0.4 mg/kg) produced a dose-dependent, transient worsening of BW performance. This reinstatement of deficits in recovered rats suggests that integrity of the α-NE system is necessary for maintaining functional recovery.

摘要

在右侧感觉运动皮层消融后 24 小时，经过训练在狭窄高架梁上行走的大鼠接受单次腹腔内注射 D-苯丙胺、可乐定、L-苯肾上腺素、哌唑嗪、育亨宾或生理盐水，然后在术后第 16 天测试其恢复在梁上行走（BW）的能力。可乐定、哌唑嗪和 L-苯肾上腺素对 BW 恢复没有明显影响。育亨宾 10mg/kg 剂量显著加速 BW 恢复，D-苯丙胺（2mg/kg）也是如此。由于 D-苯丙胺和育亨宾均可增加去甲肾上腺素（NE）释放，而先前的研究表明，在 BW 恢复中，NE 而不是多巴胺起作用，这些数据支持了这样一种假设，即增加 NE 释放有益于皮质损伤模型中的功能恢复。然而，不能排除 D-苯丙胺或育亨宾治疗的多巴胺能或 5-羟色胺能影响的可能性。为了研究 NE 系统在维持恢复中的作用，在受伤后 18 天从 BW 缺陷中恢复的动物接受可乐定、哌唑嗪或育亨宾治疗，并在 BW 任务上重新进行测试。α1-NE 拮抗剂哌唑嗪（2 或 4mg/kg）和α2-NE 激动剂可乐定（0.1 或 0.4mg/kg）均产生剂量依赖性、短暂的 BW 表现恶化。在恢复大鼠中重新出现的这些缺陷表明，α-NE 系统的完整性对于维持功能恢复是必要的。