Interferon as an endocoids candidate preventing and attenuating opiate addiction.
Morphine exert numerous effects of all levels of the central nervous system with tolerance, physical dependence and withdrawal being characteristic of this drug class. The degree of dependence is directly correlated to the intensity of withdrawal, success in modifying the withdrawal syndrome may shed light on the dynamic of morphine addiction. The present study demonstrated that alpha-interferon (IFN) significantly modifies the naloxone-induced abstinence syndrome in morphine dependent rats. Single cortical neurons recording and microiontophoretic application of IFN, morphine and naloxone failed to support existing hypothesis that IFN effects are mediated through opiate receptors. Since IFN's are widely present in animals bodies, including the brain, and are locally synthesized. Our observation suggests that IFN's are endocoids which serve to prevent tolerance and dependence to endogenous peptides.
D000818:Animals; D004553:Electric Conductivity / Q000187:drug effects; D004558:Electric Stimulation; D007370:Interferon Type I / Q000494:pharmacology*; D008297:Male; D009020:Morphine / Q000494:pharmacology; D009021:Morphine Dependence / Q000503:physiopathology*; D009043:Motor Activity / Q000187:drug effects*; D009270:Naloxone / Q000494:pharmacology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D013003:Somatosensory Cortex / Q000187:drug effects / Q000502:physiology*; D013239:Stereotyped Behavior / Q000187:drug effects*
D007370:Interferon Type I; D009270:Naloxone; D009020:Morphine