| First Author | Aoki T | Year | 2003 |
| Journal | Neurosci Lett | Volume | 350 |
| Issue | 2 | Pages | 69-72 |
| PubMed ID | 12972155 | Mgi Jnum | J:107958 |
| Mgi Id | MGI:3622593 | Doi | 10.1016/s0304-3940(03)00829-2 |
| Citation | Aoki T, et al. (2003) Disruption of the type 1 inositol 1,4,5-trisphosphate receptor gene suppresses the morphine-induced antinociception in the mouse. Neurosci Lett 350(2):69-72 |
| abstractText | The present study was designed to investigate whether endoplasmic inositol 1,4,5-trisphosphate (IP3) receptor-mediated intracellular signaling pathway could be involved in the morphine-induced antinociception in the mouse. An intracerebroventricular (i.c.v.) pretreatment with xestospongin C (10-100 pmol per mouse, i.c.v.), a membrane permeable and selective antagonist for IP3 receptor, produced a dose-dependent reduction in the supraspinal antinociceptive effect produced by i.c.v. administration of morphine (0.3-10 nmol). In addition, the dose-response curve for morphine-induced antinociception was significantly shifted to the right by i.c.v. pretreatment with xestospongin C at 100 pmol. In the present study, we confirmed that the IP3R1 mRNA in opisthonos (opt) heterozygote mice was approximately 50% reduced as compared to that in wild-type mice. Under these conditions, a significant antinociception produced by subcutaneous (s.c.) injection of morphine (5 mg/kg) observed in wild-type mice was markedly reduced in opt heterozygote mice. These findings suggest that IP3 receptor-, especially type 1 IP3 receptor-mediated intracellular signaling pathway may be implicated in the expression of antinociceptive effect induced by morphine in mice. |
