Effect of naloxone-reversible immobilization stress on the adrenal acetylcholinesterase activity in mice.
In male mice immobilized during 30 min, statistically significant increase in adrenal acetylcholinesterase (Ache) activity--up to 154% of control value--has been observed. Naloxone pretreatment (10 mg/kg b.w., ip.) suppressed that increase, Ache activity remaining at the level of non-immobilized, saline treated mice. This suggests the role of opioid peptides in this change. Ganglionic blockade by hexamethonium markedly inhibited Ache activity in adrenals of non-immobilized and of immobilized mice. Opioid peptides secreted from the splanchnic nerve terminals seem to be involved in the control of cholinergic mechanisms.
Konecka
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Department of Behavioral Physiology, Polish Academy of Sciences.
D000110:Acetylcholinesterase / Q000378:metabolism*; D000311:Adrenal Glands / Q000201:enzymology*; D000818:Animals; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D018738:Hexamethonium; D006584:Hexamethonium Compounds / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D051379:Mice; D009270:Naloxone / Q000494:pharmacology*; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000201:enzymology* / Q000209:etiology
D002800:Cholinesterase Inhibitors; D006584:Hexamethonium Compounds; D009270:Naloxone; D018738:Hexamethonium; D000110:Acetylcholinesterase