Effect of morphine on acetylcholine content of electrically stimulated brain slices.
Acetylcholine (ACh) levels were measured in guinea-pig thalamic and caudatal slices kept at rest or electrically stimulated for different times (2-30 min.). The decrease of ACh content caused by electrical pulses at 1 Hz and 2 Hz in caudate nucleus and thalamus slices, respectively, was directly related to the time of stimulation. The depletion was potentiated by HC-3 10 microM. In this condition the relationship between ACh content and time of stimulation was shifted to the left. In the presence of HC-3, Morphine (Mo) 30 microM did not affect the ACh levels of thalamic and caudatal slices kept at rest. The opioid, on the contrary, reduced the depletion of ACh caused by 10 min stimulation. Naloxone (Nx) 10 microM antagonized the opioid effect in caudate nucleus, while it increased the stimulus-induced ACh depletion in the thalamus treated with Morphine 30 microM. In conclusion, the electrically-stimulated brain tissue perfused with HC-3 may be a suitable tool to study drug effects on ACh depletion. This may offer an indirect, mirror-like evaluation of ACh apparent turnover and release. The results obtained with Mo and Nx support this statement.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000502:physiology; D002421:Caudate Nucleus / Q000378:metabolism; D004558:Electric Stimulation; D005260:Female; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D009020:Morphine / Q000494:pharmacology*; D009270:Naloxone / Q000494:pharmacology; D013788:Thalamus / Q000378:metabolism
D009270:Naloxone; D009020:Morphine; D000109:Acetylcholine