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.
Dixon
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Department of Neurosurgery, University of Pittsburgh Medical Center, PA 15260, USA. edixon@neuronet.pitt.edu
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D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001930:Brain Injuries / Q000378:metabolism*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D018680:Cholinergic Antagonists / Q000494:pharmacology; D004396:Coloring Agents; D005110:Extracellular Space / Q000187:drug effects / Q000378:metabolism; D008297:Male; D017551:Microdialysis; D018727:Muscarinic Antagonists / Q000494:pharmacology; D010275:Parasympathetic Nervous System / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000378:metabolism; D012601:Scopolamine / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
D018680:Cholinergic Antagonists; D004396:Coloring Agents; D018727:Muscarinic Antagonists; D011950:Receptors, Cholinergic; D012601:Scopolamine; D000109:Acetylcholine