Reduced evoked release of acetylcholine in the rodent neocortex following traumatic brain injury.

Neocortical acetylcholine (ACh) release was examined in awake, freely-moving rats at 14 days following lateral controlled cortical impact. Extracellular ACh was measured prior to and after an intraperitoneal administration of scopolamine, which evokes ACh release by blocking autoreceptors. At 14 days post-injury there was a significant reduction in scopolamine-evoked ACh release. The data suggest that neocortical cholinergic neurotransmission is chronically compromised, and may contribute to post-traumatic memory deficits.