Abstract
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.
Publication types
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Acetylcholine / metabolism*
-
Animals
-
Brain Injuries / metabolism*
-
Cerebral Cortex / drug effects
-
Cerebral Cortex / metabolism*
-
Cholinergic Antagonists / pharmacology
-
Coloring Agents
-
Extracellular Space / drug effects
-
Extracellular Space / metabolism
-
Male
-
Microdialysis
-
Muscarinic Antagonists / pharmacology
-
Parasympathetic Nervous System / drug effects
-
Parasympathetic Nervous System / physiology
-
Rats
-
Rats, Sprague-Dawley
-
Receptors, Cholinergic / drug effects
-
Receptors, Cholinergic / metabolism
-
Scopolamine / pharmacology
-
Synaptic Transmission / drug effects
-
Synaptic Transmission / physiology
Substances
-
Cholinergic Antagonists
-
Coloring Agents
-
Muscarinic Antagonists
-
Receptors, Cholinergic
-
Scopolamine
-
Acetylcholine