Depletion of choline acetyltransferase activity but preservation of M1 and M2 muscarinic receptor binding sites in temporal cortex following head injury: a preliminary human postmortem study.

Abnormalities of cholinergic neurotransmission have been implicated in the memory deficits that result from head injury on the basis of results obtained from experimental animal models and cholinergic agonist treatment in head-injured survivors. The purpose of the present study was to make a preliminary investigation of pre- and postsynaptic markers of cholinergic transmission in human postmortem brain from patients who died as a result of head injury and age matched controls. Choline acetyltransferase activity, M1 and M2 receptor binding sites were assayed in the inferior temporal gyrus from 7 head-injured patients and 7 controls. The mean value of choline acetyltransferase activity was reduced by approximately 50% in the head-injured group compared to the control, although in 2 head-injured cases enzyme activity was similar to that of controls. In contrast to the reduction in choline acetyltransferase activity, there was no difference between the head-injured and control groups in the levels of either M1 or M2 receptor binding. These preliminary results indicate that there is a significant presynaptic abnormality of cholinergic neurotransmission in postmortem human brain following head injury but that muscarinic receptor binding sites are unaltered.

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