Abstract

The importance of cholinergic transmission in the mechanisms of awakening and orientation is well known. There is general agreement that the postural atonia and coma that are observed in the postconcussion period can be induced by microinjection of cholinergic agents into the pontine tegmentum. Also, the fact that glucose utilization increases in the pontine tegmentum following cerebral concussion suggests that there is an important relationship between cerebral concussion and cholinergic activation in the central nervous system. In this study the levels and turnover rate of acetylcholine (ACh) were measured in rats at 12 minutes and 4 hours following experimental head injury. The measurements, which were compared with those in control rats, were made in the basal forebrain, thalamus, hypothalamus, frontal cortex, amygdala, hippocampus, and pontine tegmenturn by the fluid percussion method. Injured rats exhibited nonfatal, reversible neurological suppression classified as severe concussion. During the period of concussive neurological suppression, ACh levels significantly increased in the hippocampus and pontine tegmentum, but the turnover rate of ACh was accelerated only in the basal forebrain and pontine tegmentum. At 4 hours post-injury, there was no significant change in the turnover rate of ACh in any of the seven sites studied, nor was the averaged ACh turnover rate in these seven areas. These results suggest that increased cholinergic activity in the basal forebrain and pontine tegmenturn following cerebral concussion may be one cause of concussive neurological suppression.

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