HYPOTHERMIA BLUNTS ACETYLCHOLINE INCREASE IN CSF OF TRAUMATICALLY BRAIN INJURED RATS

Activation of muscarinic acetylcholine (ACh) receptors contributes to the pathophysiological consequences of moderate experimental traumatic brain injury (TBI). Hypothermia (30-degrees-C) provides protection in experimental TBI. We measured ACh levels in CSF and plasma 5 min afte r moderate fluid percussion TBI under normothermic or hypothermic cond itions, because ACh in the CSF has been correlated with the severity o f behavioral deficits after TBI. Three groups were examined: TBI with hypothermic brain (30-degrees-C), TBI with normothermic brain (37-degr ees-C), or sham TBI with normothermic brain (37-degrees-C). ACh concen trations in CSF were significantly higher in 37-degrees-C TBI rats, bu t not in 30-degrees-C TBI rats compared to shams. ACh concentratons in plasma did not differ between groups. These results suggest that a co ntributing factor to the neuroprotective effects of moderate hypotherm ia in TBI may be related to the reduction of excessive ACh levels in t he central nervous system following injury.