PMID- 9878862
OWN - NLM
STAT- MEDLINE
DCOM- 19990226
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 815
IP  - 2
DP  - 1999 Jan 9
TI  - Role of intracellular calcium on the modulation of naloxone-precipitated 
      withdrawal jumping in morphine-dependent mice by diabetes.
PG  - 424-30
AB  - 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.
CI  - Copyright 1999 Elsevier Science B.V.
FAU - Ohsawa, M
AU  - Ohsawa M
AD  - Department of Pathophysiology and Therapeutics, Faculty of Pharmaceutical 
      Sciences, 4-41, Ebara 2-Chome, Shinagawa-ku, Hoshi University, Tokyo 142, Japan.
FAU - Kamei, J
AU  - Kamei J
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 36B82AMQ7N (Naloxone)
RN  - 76I7G6D29C (Morphine)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Behavior, Animal/drug effects
MH  - Calcium/*physiology
MH  - Diabetes Mellitus, Experimental/*metabolism/physiopathology
MH  - Injections, Intraventricular
MH  - Injections, Subcutaneous
MH  - Intracellular Fluid/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Morphine/*administration & dosage
MH  - Naloxone/*administration & dosage
MH  - Substance Withdrawal Syndrome/*metabolism/physiopathology
EDAT- 1999/01/08 00:00
MHDA- 1999/01/08 00:01
CRDT- 1999/01/08 00:00
PHST- 1999/01/08 00:00 [pubmed]
PHST- 1999/01/08 00:01 [medline]
PHST- 1999/01/08 00:00 [entrez]
AID - S0006-8993(98)01109-3 [pii]
AID - 10.1016/s0006-8993(98)01109-3 [doi]
PST - ppublish
SO  - Brain Res. 1999 Jan 9;815(2):424-30. doi: 10.1016/s0006-8993(98)01109-3.