In rats, an ED50 for analgesia of morphine, meperidine, viminol R2 or azidomorphine decreases the turnover rate of acetylcholine (TR(ACh)) in cortex and hippocampus. These four analgetics fail to change the TR (ACh) in striatum when given in a dose range from ED30 for analgesia up to a cataleptic dose. Viminol S2, a nonanalgesic stereoisomer of viminol R2, fails to decrease the TR(ACh) in cortex and hippocampus. Naltrexone, an opiate antagonist, also fails to change the cortical and hippocampal TR (ACh) but it antagonizes the decrease in cortical and hippocampal TR(ACh) elicited by the four analgetics. Since the ED50 of these four analgetics fails to change the TR(ACh) in striatum which contains a high density of opiate receptors and intrinsic cholinergic neurons, but decreases the TR(ACh) in hippocampus and cortex which contain a low density of opiate receptors, it can be inferred that opiate receptors are not exclusively involved in the regulation of TR(ACh). However, the results suggest that certain cholinergic pathways participate in the mediation of analgesia.
|Number of pages||7|
|Journal||Journal of Pharmacology and Experimental Therapeutics|
|Publication status||Published - Dec 1 1976|
ASJC Scopus subject areas
- Molecular Medicine