Affiliations: Departments of Psychology and Physiology, The University of New Mexico, Albuquerque, NM 87131 (U.S.A.)
Note: [] Correspondence: R.L. Sutton, The University of New Mexico, School of Medicine, Division of Neurosurgery, Albuquerque, NM 87131, U.S.A.
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.
Keywords: α1,2-Agonists, α1,2-Antagonists, Brain injury, Hemiplegia, Norepinephrine, Recovery of function, Sensorimotor cortex, Reinstatement of deficits
