Effect of diabetes on the antinociceptive effect of β-endorphin

• Published in: Brain research Vol. 619; no. 1; pp. 76 - 80
• Main Authors: Kamei, Junzo, Kawashima, Naoya, Hitosugi, Hideki, Misawa, Miwa, Nagase, Hiroshi, Kasuya, Yutaka
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 13.08.1993; Amsterdam Elsevier; New York, NY
• Subjects: 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; Analgesics; Analgesics - pharmacology; Animals; Antinociception; beta-Endorphin - administration & dosage; beta-Endorphin - pharmacology; Biological and medical sciences; Cerebral Ventricles - drug effects; Cerebral Ventricles - physiology; Cerebral Ventricles - physiopathology; DAMGO; Diabetes; Diabetes Mellitus, Experimental - physiopathology; Dose-Response Relationship, Drug; DPDPE; Enkephalin, Ala-MePhe-Gly; Enkephalin, D-Penicillamine (2,5); Enkephalins - pharmacology; Injections, Intraventricular; Male; Medical sciences; Mice; Mice, Inbred ICR; Mouse; Naltrexone - administration & dosage; Naltrexone - analogs & derivatives; Naltrexone - pharmacology; Naltrindole; Narcotic Antagonists - pharmacology; Neuropharmacology; Pain - physiopathology; Pain - prevention & control; Pharmacology. Drug treatments; Pyrrolidines - pharmacology; Reference Values; U-50,488H; β-Endorphin; DAMGO; Mouse; U-50,488H; Antinociception; Naltrindole; Diabetes; β-Endorphin; DPDPE; Endocrinopathy; Nociception; Diabetes mellitus; Rodentia; Opioid peptide; Intrathecal administration; Opiate receptor; Analgesia; Vertebrata; Experimental disease; Mammalia; Analgesic; Animal; Intracerebral administration
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/0006-8993(93)91597-L

We examined whether streptozotocin-induced diabetes can modulate β-endorphin-induced antinociception in mice. While β-endorphin administered i.c.v. produced a dose-dependent inhibition of the tail-flick response in both diabetic and non-diabetic mice, the antinociceptive response was greater in diabetic mice than in non-diabetic mice. The ED 50 value of β-endorphin administered i.c.v. in diabetic mice was significantly lower than that in non-diabetic mice. The antinociceptive effects of β-endorphin administered i.c.v. in both diabetic and non-diabetic mice were significantly antagonized by s.c. administration of naltrindole, a selective δ-opioid receptor antagonist. β-Endorphin administered i.t. also produced a dose-dependent antinociception in both diabetic and non-diabetic mice. However, the ED 50 value of β-endorphin administered i.t. in diabetic mice was significantly higher than that in non-diabetic mice. The antinociceptive effect of β-endorphin administered i.t. in both diabetic and non-diabetic mice were significantly antagonized by s.c. administration of nor-binaltorphimine, a selective κ-opioid receptor antagonist. On the other hand, the antinociceptive potency of DPDPE, a selective δ-opioid agonist, administered i.t. is significantly increased in diabetic mice, as compared with non-diabetic mice, whereas, the antinociceptive potency of U-50,488H, a κ-opioid receptor agonist, administered i.t. is significantly less than in non-diabetic mice. These results suggest that diabetes may modulate β-endorphin-induced antinociception differently at the spinal and supraspinal levels.