Abstract
Objective: The cholinergic system is highly vulnerable to traumatic brain injury (TBI). However, limited information is available to what extent the degrading enzyme acetylcholinesterase (AChE) is involved. The present study addresses this question.Method: Thirty-six anaesthetized Sprague-Dawley rats were subjected to sham operation or to TBI using controlled cortical impact (CCI). The AChE activity was histochemically determined in frozen brain slices at 2, 24 and 72 hours after TBI.Results: High enzyme activity was observed in regions rich in cholinergic innervation such as the olfactory tubercle, basal forebrain, putamen and superior colliculi. Low activity was found in the cortex, cerebellum and particularly in the white matter. A decrease of AchE activity (20–35%) was found in the hippocampus and hypothalamus already at 2 hours after TBI. An increase of ∼30% was found in the basal forebrain at 2 and 24 hours. No changes occurred at 72 hours.Conclusion: The findings are consistent with impairment of the cholinergic neurotransmission after TBI and suggest the involvement of the AChE in short-term regulatory mechanisms.
Published Version
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