TRAUMATIC BRAIN INJURY REDUCES HIPPOCAMPAL HIGH-AFFINITY [H-3] CHOLINE UPTAKE BUT NOT EXTRACELLULAR CHOLINE LEVELS IN RATS

Hippocampal cholinergic hypofunction may contribute to memory deficits following experimental traumatic brain injury. These studies examined two important factors in acetylcholine synthesis: choline availabilit y and neuronal uptake. No reductions in basal extracellular choline le vels, using microdialysis, were observed 2 weeks after cortical impact injury. However, studies of high affinity [H-3]choline uptake in the hippocampus, measured in a synaptosomal preparation, found a reduction in the maximum velocity of choline uptake (V-max), while no differenc es in affinity constants (K-m) were found. The results suggest that po st-traumatic cholinergic deficits are not attributable to decreased av ailability of choline, but may be associated with either a decreased a bility of cholinergic neurons to take up choline and/or a loss of chol inergic neurons.