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- Title
Dual effect of cAMP agonist on ameliorative function of PKA inhibitor in morphine-dependent mice.
- Authors
Seyedi, Seyedeh Y.; Salehi, Forouz; Payandemehr, Borna; Hossein, Sara; Hosseini‐Zare, Mahshid S.; Nassireslami, Ehsan; Yazdi, Behnoosh B.; Sharifzadeh, Mohammad
- Abstract
The present study shows interactive effects of bucladesine (db- cAMP) as a cyclic adenosine monophosphate ( cAMP) agonist and H-89 as a protein kinase A ( PKA) inhibitor on naloxone-induced withdrawal signs in morphine-dependent mice. Animals were treated subcutaneously with morphine thrice daily with doses progressively increased from 50 to 125 mg/kg. A last dose of morphine (50 mg/kg) was administered on the 4th day. Several withdrawal signs were precipitated by intraperitoneal (i.p.) administration of naloxone (5 mg/kg). Different doses of bucladesine (50, 100, 200 n m/mouse) and H-89 (0.05, 0.5, 1, 5 mg/kg) were administered (i.p.) 60 min before naloxone injection. In combination groups, bucladesine was injected 15 min before H-89 injection. Single administration of H-89 (0.5, 1, 5 mg/kg) and bucladesine (50, 100 n m/mouse) significantly attenuated prominent behavioral signs of morphine withdrawal. Lower doses of bucladesine (50, 100 n m/mouse) in combination with H-89 (0.05 mg/kg) increased the inhibitory effects of H-89 on withdrawal signs while in high dose (200 n m/mouse) decreased the ameliorative function of H-89 (0.05 mg/kg) in morphine-dependent animals. It is concluded that H-89 and bucladesine could affect morphine withdrawal syndrome via possible interaction with cyclic nucleotide messengering systems, protein kinase A signaling pathways, and modified related neurotransmitters.
- Subjects
CYCLIC adenylic acid; CYCLIC-AMP-dependent protein kinase; NALOXONE; MORPHINE; NEUROTRANSMITTERS; LABORATORY mice
- Publication
Fundamental & Clinical Pharmacology, 2014, Vol 28, Issue 4, p445
- ISSN
0767-3981
- Publication type
Article
- DOI
10.1111/fcp.12045