A single dose of an alpha1-noradrenergic antagonist transiently reinstates
hemiplegia after recovery from
brain injury, which suggests that
noradrenaline (NA) is required to maintain recovery. No systematic studies have determined the postinjury duration of this vulnerability. This study used a within-subject, dose-response design to determine whether
prazosin (PRAZ), an alpha1-NA antagonist, or
propranolol (PROP), a beta-NA antagonist, would continue to reinstate
hemiplegia over time after recovery from weight-drop
traumatic brain injury (TBI). PRAZ transiently reinstated
hemiplegia as measured by beam walk (BW) score in a dose-dependent manner, with the same degree of symptom reinstatement at 1, 3, 6, and 12 months post-TBI. Between-animal variability in reinstatement of
hemiplegia by PRAZ was predicted by severity of deficits in BW ability 24 h after TBI. In contrast, PRAZ did not reinstate tactile placing deficits at 1 month post-TBI suggesting a different mechanism of maintaining recovery for each task. Reinstatement of symptoms are not due to sedation. Only TBI rats receiving PRAZ, not high, sedating doses of PROP or saline (SAL), showed return of
hemiplegia. These data indicate that vulnerability to transient reinstatement of
hemiplegia on some tasks endures long after functional recovery from TBI.