Tags

Type your tag names separated by a space and hit enter

Involvement of central opioid systems in human interferon-alpha induced immobility in the mouse forced swimming test.
Br J Pharmacol. 2000 Jul; 130(6):1269-74.BJ

Abstract

1. We investigated the mechanism by which human interferon-alpha (IFN-alpha) increases the immobility time in a forced swimming test, an animal model of depression. 2. Central administration of IFN-alpha (0.05 - 50 IU per mouse, i.cist.) increased the immobility time in the forced swimming test in mice in a dose-dependent manner. 3. Neither IFN-beta nor -gamma possessed any effect under the same experimental conditions. 4. Pre-treatment with an opioid receptor antagonist, naloxone (1 mg kg(-1), s.c.) inhibited the prolonged immobility time induced by IFN-alpha (60 KIU kg(-1), i.v. or 50 IU per mouse. i.cist.). 5. Peripheral administration of naloxone methiodide (1 mg kg(-1), s. c.), which does not pass the blood - brain barrier, failed to block the effect of IFN-alpha, while intracisternal administration of naloxone methiodide (1 nmol per mouse) completely blocked. 6. The effect of IFN-alpha was inhibited by a mu(1)-specific opioid receptor antagonist, naloxonazine (35 mg kg(-1), s.c.) and a mu(1)/mu(2) receptor antagonist, beta-FNA (40 mg kg(-1), s.c.). A selective delta-opioid receptor antagonist, naltrindole (3 mg kg(-1), s.c.) and a kappa-opioid receptor antagonist, nor-binaltorphimine (20 mg kg(-1), s.c.), both failed to inhibit the increasing effect of IFN-alpha. 7. These results suggest that the activator of the central opioid receptors of the mu(1)-subtype might be related to the prolonged immobility time of IFN-alpha, but delta and kappa-opioid receptors most likely are not involved.

Authors+Show Affiliations

Drug Safety Research Laboratory, Daiichi Pharmaceutical Co., Ltd., Tokyo, Japan. makinald@daiichipharm.co.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

10903965

Citation

Makino, M, et al. "Involvement of Central Opioid Systems in Human Interferon-alpha Induced Immobility in the Mouse Forced Swimming Test." British Journal of Pharmacology, vol. 130, no. 6, 2000, pp. 1269-74.
Makino M, Kitano Y, Komiyama C, et al. Involvement of central opioid systems in human interferon-alpha induced immobility in the mouse forced swimming test. Br J Pharmacol. 2000;130(6):1269-74.
Makino, M., Kitano, Y., Komiyama, C., Hirohashi, M., & Takasuna, K. (2000). Involvement of central opioid systems in human interferon-alpha induced immobility in the mouse forced swimming test. British Journal of Pharmacology, 130(6), 1269-74.
Makino M, et al. Involvement of Central Opioid Systems in Human Interferon-alpha Induced Immobility in the Mouse Forced Swimming Test. Br J Pharmacol. 2000;130(6):1269-74. PubMed PMID: 10903965.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of central opioid systems in human interferon-alpha induced immobility in the mouse forced swimming test. AU - Makino,M, AU - Kitano,Y, AU - Komiyama,C, AU - Hirohashi,M, AU - Takasuna,K, PY - 2000/7/25/pubmed PY - 2000/9/19/medline PY - 2000/7/25/entrez SP - 1269 EP - 74 JF - British journal of pharmacology JO - Br J Pharmacol VL - 130 IS - 6 N2 - 1. We investigated the mechanism by which human interferon-alpha (IFN-alpha) increases the immobility time in a forced swimming test, an animal model of depression. 2. Central administration of IFN-alpha (0.05 - 50 IU per mouse, i.cist.) increased the immobility time in the forced swimming test in mice in a dose-dependent manner. 3. Neither IFN-beta nor -gamma possessed any effect under the same experimental conditions. 4. Pre-treatment with an opioid receptor antagonist, naloxone (1 mg kg(-1), s.c.) inhibited the prolonged immobility time induced by IFN-alpha (60 KIU kg(-1), i.v. or 50 IU per mouse. i.cist.). 5. Peripheral administration of naloxone methiodide (1 mg kg(-1), s. c.), which does not pass the blood - brain barrier, failed to block the effect of IFN-alpha, while intracisternal administration of naloxone methiodide (1 nmol per mouse) completely blocked. 6. The effect of IFN-alpha was inhibited by a mu(1)-specific opioid receptor antagonist, naloxonazine (35 mg kg(-1), s.c.) and a mu(1)/mu(2) receptor antagonist, beta-FNA (40 mg kg(-1), s.c.). A selective delta-opioid receptor antagonist, naltrindole (3 mg kg(-1), s.c.) and a kappa-opioid receptor antagonist, nor-binaltorphimine (20 mg kg(-1), s.c.), both failed to inhibit the increasing effect of IFN-alpha. 7. These results suggest that the activator of the central opioid receptors of the mu(1)-subtype might be related to the prolonged immobility time of IFN-alpha, but delta and kappa-opioid receptors most likely are not involved. SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/10903965/Involvement_of_central_opioid_systems_in_human_interferon_alpha_induced_immobility_in_the_mouse_forced_swimming_test_ L2 - https://doi.org/10.1038/sj.bjp.0703432 DB - PRIME DP - Unbound Medicine ER -