Dicyclomine (1 mg/kg or 10 mg/kg),
scopolamine (1 mg/kg), or saline was administered intraperitoneally to rats 15 min prior to moderate fluid percussion
brain injury. A variety of reflexes and responses were measured up to 60 min following injury, and
body weight and several neurological measures were taken daily up to 10 days following injury. All 3
antimuscarinic treatments reduced the duration of transient behavioral suppression as assessed by these measures. It appears that blockade of the
M1 muscarinic receptor can attenuate transient behavioral suppression associated with concussive
brain injury. Thus, stimulation of
M1 muscarinic receptors may mediate components of reversible traumatic unconsciousness following
cerebral concussion. No differences were observed between saline and
antimuscarinic treatments in the incidence or duration of
apnea following injury.
Scopolamine pretreatment significantly elevated heart rate prior to injury, but had no significant effect on the responses of heart rate and blood pressure to experimental concussion. Both doses of
dicyclomine significantly reduced resting heart rate, but unlike
scopolamine, significantly enhanced the cardiovascular response to fluid percussion injury.
Antimuscarinic treatment significantly reduced
body weight loss and certain motor deficits, including beam balance and beam walk performance, following concussive
head injury.
Scopolamine and both doses of
dicyclomine appeared to be equally effective in reducing long-term deficits. Data from these experiments indicate that at least some of the long-term behavioral deficits following moderate levels of
brain injury may involve the binding of
acetylcholine to
M1 muscarinic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)