PMID- 10810247
OWN - NLM
STAT- MEDLINE
DCOM- 20000711
LR  - 20190607
IS  - 1021-7770 (Print)
IS  - 1021-7770 (Linking)
VI  - 7
IP  - 3
DP  - 2000 May-Jun
TI  - The nucleus paragigantocellularis and opioid withdrawal-like behavior.
PG  - 270-6
AB  - Participation of the nucleus paragigantocellularis (PGi) in mediation of opioid 
      withdrawal was examined in conscious, unrestrained, non-opioid-dependent rats, 
      using electrical stimulation of the PGi. A characteristic series of behaviors, 
      which resembled those seen during naloxone-precipitated withdrawal from 
      dependence on the opioid agonist, butorphanol, was elicited during 30 min of PGi 
      stimulation. Thus, the behavioral syndrome has been termed opioid 
      withdrawal-like. Simultaneous microdialysis measurement of glutamate within the 
      locus ceruleus indicated a positive correlation between extracellular glutamate 
      concentrations and behavioral responses. Behavioral responses were inhibited by 
      50% during reverse dialysis perfusion of the locus ceruleus with the glutamate 
      receptor antagonist, kynurenic acid, without any effect on glutamate 
      concentrations. Thus, increases in locus ceruleus glutamate partially mediate 
      opioid withdrawal-like behavior. Intracerebroventricular (i.c.v.) injections of 
      the opioid antagonist, naloxone, or of the mu-selective (beta-funaltrexamine) or 
      the delta-selective (naltrindole) opioid antagonists decreased, but did not 
      abolish, stimulation-induced behavioral responses. Similar i.c.v. injections of 
      the kappa-selective antagonist, nor-binaltorphimine, had no effect on behavioral 
      responses to PGi stimulation. Activation of the PGi by electrical stimulation can 
      elicit behaviors similar to those observed during opioid withdrawal. Moreover, 
      additional levels of complexity are evident in the neuropharmacology of PGi 
      stimulation-induced opioid withdrawal-like behavior.
FAU - Rockhold, R W
AU  - Rockhold RW
AD  - Department of Pharmacology and Toxicology, University of Mississippi Medical 
      Center, Jackson, Miss. 39216-4505, USA. rrockhold@pharmacology.umsmed.edu
FAU - Liu, N
AU  - Liu N
FAU - Coleman, D
AU  - Coleman D
FAU - Commiskey, S
AU  - Commiskey S
FAU - Shook, J
AU  - Shook J
FAU - Ho, I K
AU  - Ho IK
LA  - eng
GR  - DA-05828/DA/NIDA NIH HHS/United States
GR  - GM-08110/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Biomed Sci
JT  - Journal of biomedical science
JID - 9421567
RN  - 0 (Narcotic Antagonists)
RN  - 0 (Narcotics)
RN  - 0RH81L854J (Glutamine)
RN  - 36B82AMQ7N (Naloxone)
RN  - 36OOQ86QM1 (norbinaltorphimine)
RN  - 451W47IQ8X (Sodium Chloride)
RN  - 5S6W795CQM (Naltrexone)
RN  - 72782-05-9 (beta-funaltrexamine)
RN  - G167Z38QA4 (naltrindole)
RN  - QV897JC36D (Butorphanol)
SB  - IM
MH  - Animals
MH  - Behavior, Animal/drug effects/physiology
MH  - Butorphanol/adverse effects
MH  - Electric Stimulation
MH  - Glutamine/metabolism
MH  - Male
MH  - Medulla Oblongata/*physiology
MH  - Naloxone/pharmacology
MH  - Naltrexone/analogs & derivatives/pharmacology
MH  - Narcotic Antagonists/pharmacology
MH  - Narcotics/*adverse effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sodium Chloride/pharmacology
MH  - *Substance Withdrawal Syndrome/physiopathology
MH  - Synaptic Transmission/drug effects
MH  - Time Factors
EDAT- 2000/05/16 09:00
MHDA- 2000/07/15 11:00
CRDT- 2000/05/16 09:00
PHST- 2000/05/16 09:00 [pubmed]
PHST- 2000/07/15 11:00 [medline]
PHST- 2000/05/16 09:00 [entrez]
AID - 25458 [pii]
AID - 10.1007/BF02255476 [doi]
PST - ppublish
SO  - J Biomed Sci. 2000 May-Jun;7(3):270-6. doi: 10.1007/BF02255476.