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pubmed-article:2067975pubmed:abstractTextThe effects of two endogenous mammalian FMRFamide (Phe-Met-Arg-Phe-NH2)-related peptides, an octapeptide F8Fa (Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-NH2) and an octadecapeptide A18Fa (Ala-Gly-Glu-Gly-Leu-Ser-Ser-Pro-Phe-Trp-Ser-Leu-Ala-Pro-Gln-Arg-Phe-NH2 ), and IgG from serum against them on the responses to aggression and defeat-induced analgesia were examined in subordinate mice in "resident-intruder" pairings. Intracerebroventricular (ICV) administrations of F8Fa and A18Fa (0.10-10 micrograms) reduced, in a dose-dependent manner, the number of bites to obtain defeat in the subordinate mice during the agonistic encounters, as well as attenuating defeat-induced analgesia, with F8Fa having a greater inhibitory effect than A18Fa. Peripheral administration of naloxone (1.0 mg/kg) had a similar inhibitory effect on the number of bites to defeat and the level of defeat-induced analgesia. In contrast, ICV administrations of F8Fa-IgG and A18Fa-IgG antisera increased the number of bites to defeat and augmented the levels of defeat-induced analgesia, with F8Fa-IgG having a greater effect than A18Fa-IgG. These results provide further evidence that the peptides, F8Fa and A18Fa, are involved in the modulation of opioid-mediated analgesia accompanying biological stressors and suggest that these endogenous FMRF-NH2-related peptides may also be associated with the expression of opioid-sensitive components of aggressive behavior.lld:pubmed
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pubmed-article:2067975pubmed:authorpubmed-author:YangH YHYlld:pubmed
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pubmed-article:2067975pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:2067975pubmed:articleTitleEffects of mammalian FMRF-NH2-related peptides and IgG from antiserum against them on aggression and defeat-induced analgesia in mice.lld:pubmed
pubmed-article:2067975pubmed:affiliationDivision of Oral Biology, Faculty of Dentistry, University of Western Ontario, London, Canada.lld:pubmed
pubmed-article:2067975pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:2067975pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed