title: Role of intracellular calcium on the modulation of naloxone-precipitated withdrawal jumping in morphine-dependent mice by diabetes.
abstract: The role of intracellular calcium in the modifications of naloxone-precipitated withdrawal jumping in morphine-dependent mice by diabetes was examined. Naloxone-precipitated withdrawal jumping was significantly less in morphine-dependent diabetic mice than in morphine-dependent non-diabetic mice. Intracerebroventricular (i.c.v. ) pretreatment with ryanodine attenuated naloxone-precipitated withdrawal jumping in morphine-dependent non-diabetic mice. However, naloxone-precipitated withdrawal jumping in morphine-dependent diabetic mice was not affected by i.c.v. pretreatment with ryanodine. Moreover, i.c.v. pretreatment with thapsigargin, a Ca2+-ATPase inhibitor, enhanced naloxone-precipitated withdrawal jumping in morphine-dependent non-diabetic mice, but not in morphine-dependent diabetic mice. The noradrenaline (NA) turnover in the frontal cortex in morphine-dependent non-diabetic mice, but not in morphine-dependent diabetic mice, was significantly increased by naloxone injection. Naloxone-induced enhancement of NA turnover in morphine-dependent non-diabetic mice, but not in morphine-dependent diabetic mice, was blocked by i.c.v. pretreatment with ryanodine. In contrast to ryanodine, thapsigargin enhanced naloxone-induced enhancement of NA turnover in morphine-dependent non-diabetic mice. These results suggest that increased intracellular calcium augmented naloxone-precipitated withdrawal jumping and the turnover rate of NA in the frontal cortex in morphine-dependent non-diabetic mice. Furthermore, it seems likely that the attenuation of naloxone-precipitated withdrawal jumping in morphine-dependent diabetic mice may be due, in part, to the dysfunction of intracellular calcium store.
authors.affiliation: Department of Pathophysiology and Therapeutics, Faculty of Pharmaceutical Sciences, 4-41, Ebara 2-Chome, Shinagawa-ku, Hoshi University, Tokyo 142, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ohsawa
authors.forename: J
authors.initials: J
authors.lastname: Kamei
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D002118:Calcium / Q000502:physiology*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000503:physiopathology; D007276:Injections, Intraventricular; D007279:Injections, Subcutaneous; D007424:Intracellular Fluid / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009020:Morphine / Q000008:administration & dosage*; D009270:Naloxone / Q000008:administration & dosage*; D013375:Substance Withdrawal Syndrome / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D009270:Naloxone; D009020:Morphine; D002118:Calcium