PMID- 10708732
OWN - NLM
STAT- MEDLINE
DCOM- 20000511
LR  - 20190624
IS  - 0014-2999 (Print)
IS  - 0014-2999 (Linking)
VI  - 390
IP  - 3
DP  - 2000 Mar 3
TI  - Possible involvement of the locus coeruleus in inhibition by prostanoid EP(3) 
      receptor-selective agonists of morphine withdrawal syndrome in rats.
PG  - 257-66
AB  - We examined the mechanism of the inhibitory effect of prostanoid EP(3) receptor 
      agonists on naloxone-precipitated withdrawal syndrome in morphine-dependent rats. 
      Rats were rendered morphine dependent by subcutaneous (s.c.) implantation of two 
      pellets containing 75 mg morphine for 5 days. Morphine withdrawal syndrome was 
      precipitated by i.p. injection of naloxone (3 mg/kg). Intracerebroventricular 
      (i.c.v.) administration of (+/-)-15alpha-hydroxy-9-oxo-16-phenoxy-17,18, 
      19,20-tetranorprost-13-trans-enoic acid (M&B28,767: prostanoid EP(3) receptor 
      agonist) or sulprostone (prostanoid EP(1)/EP(3) receptor agonist) significantly 
      suppressed many withdrawal signs. Northern blotting and in situ hybridization 
      studies revealed that i.c.v. administration of M&B28,767 (1 pg/rat) attenuated 
      the elevation of c-fos mRNA during naloxone-precipitated withdrawal in many brain 
      regions, including the cerebral cortex, thalamus, hypothalamus and locus 
      coeruleus. Double in situ hybridization analysis revealed that in the locus 
      coeruleus most of the tyrosine hydroxylase mRNA-positive neurons expressed 
      mu-opioid receptor mRNA and more than half of these neurons were positive for 
      prostanoid EP(3) receptor mRNA. These results indicate that the suppression by 
      prostanoid EP(3) receptor agonists of naloxone-precipitated morphine withdrawal 
      syndrome can be attributed to the inhibition of neuronal activity in several 
      brain regions, including the locus coeruleus, the largest source of central 
      noradrenergic neurons.
FAU - Nakagawa, T
AU  - Nakagawa T
AD  - Department of Molecular Pharmacology, Faculty of Pharmaceutical Sciences, Kyoto 
      University, Kyoto, Japan.
FAU - Masuda, T
AU  - Masuda T
FAU - Watanabe, T
AU  - Watanabe T
FAU - Minami, M
AU  - Minami M
FAU - Satoh, M
AU  - Satoh M
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 0 (Ptger3 protein, rat)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Opioid, mu)
RN  - 0 (Receptors, Prostaglandin E)
RN  - 0 (Receptors, Prostaglandin E, EP3 Subtype)
RN  - 36B82AMQ7N (Naloxone)
RN  - 501Q5EQ1GM (sulprostone)
RN  - 76I7G6D29C (Morphine)
RN  - 80558-61-8 (11-deoxy-16-phenoxy-17,18,19,20-tetranorprostaglandin E1)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - F5TD010360 (Alprostadil)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Alprostadil/analogs & derivatives/pharmacology
MH  - Animals
MH  - Brain/drug effects/metabolism
MH  - Dinoprostone/analogs & derivatives/pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Gene Expression Regulation/drug effects
MH  - In Situ Hybridization
MH  - Injections, Intraventricular
MH  - Locus Coeruleus/*drug effects/metabolism
MH  - Male
MH  - Morphine/*adverse effects
MH  - Morphine Dependence/prevention & control
MH  - Naloxone/pharmacology
MH  - Proto-Oncogene Proteins c-fos/genetics
MH  - RNA, Messenger/drug effects/genetics/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Opioid, mu/genetics
MH  - Receptors, Prostaglandin E/*agonists/genetics
MH  - Receptors, Prostaglandin E, EP3 Subtype
MH  - Substance Withdrawal Syndrome/etiology/physiopathology/*prevention & control
MH  - Tyrosine 3-Monooxygenase/genetics
EDAT- 2000/03/10 09:00
MHDA- 2000/05/16 09:00
CRDT- 2000/03/10 09:00
PHST- 2000/03/10 09:00 [pubmed]
PHST- 2000/05/16 09:00 [medline]
PHST- 2000/03/10 09:00 [entrez]
AID - S0014299999009012 [pii]
AID - 10.1016/s0014-2999(99)00901-2 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2000 Mar 3;390(3):257-66. doi: 10.1016/s0014-2999(99)00901-2.