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  • 1.
    Backstrom, Tobias
    et al.
    Uppsala Univ, Dept Neurosci, Physiol Unit, Biomed Ctr BMC, SE-75123 Uppsala, Sweden / Uppsala Univ, Evolutionary Biol Ctr, SE-75236 Uppsala, Sweden .
    Pettersson, Andreas
    Swedish Univ Agr Sci, Dept Food Sci, SE-75007 Uppsala, Sweden.
    Johansson, Viktoria
    University of Skövde, School of Life Sciences.
    Winberg, Svante
    Uppsala Univ, Dept Neurosci, Physiol Unit, Biomed Ctr BMC, SE-75123 Uppsala, Sweden .
    CRF and urotensin I effects on aggression and anxiety-like behavior in rainbow trout2011In: Journal of Experimental Biology, ISSN 0022-0949, E-ISSN 1477-9145, Vol. 214, no 6, p. 907-914Article in journal (Refereed)
    Abstract [en]

    Corticotropin-releasing factor (CRF) is central in the stress response but also modulates several behaviors including anxiety-related behaviors and aggression. In this study, juvenile rainbow trout (Oncorhynchus mykiss) were tested for competitive ability, determined during dyadic fights for dominance, after intracerebroventricular (i.c.v.) administration of CRF, urotensin I (UI), the non-specific CRF antagonist alpha-helical RF(9-41) (ahCRF) or the CRF receptor subtype 1-specific antagonist antalarmin, when paired with a mass-matched con-specific injected with saline. In addition, isolated fish received the same substances. Plasma cortisol and brain monoamines were monitored in all fish. Most fish receiving CRF showed a conspicuous behavior consisting of flaring the opercula, opening the mouth and violent shaking of the head from side to side. When this occurred, the fish immediately forfeited the fight. Similar behavior was observed in most fish receiving UI but no effect on outcome of dyadic fights was noted. This behavior seems similar to non-ambulatory motor activity seen in rats and could be anxiety related. Furthermore, fish receiving CRF at a dose of 1000. ng became subordinate, whereas all other treatments had no effects on the outcome of dyadic fights. In addition, isolated fish receiving ahCRF had lower brain stem concentrations of 5-hydroxyindoleacetic acid, serotonin, 3,4-dihydroxyphenylacetic acid and dopamine. In conclusion, CRF seems to attenuate competitive ability, and both CRF and UI seem to induce anxiety-like behavior.

  • 2.
    Hagberg, Malin
    et al.
    University of Skövde, School of Life Sciences.
    Holmén, Jonathan
    University of Skövde, School of Life Sciences.
    Olausson, Josefin
    University of Skövde, School of Life Sciences.
    Karlsson, Sandra
    University of Skövde, School of Life Sciences.
    Johansson, Viktoria
    University of Skövde, School of Life Sciences.
    Larsson, Dennis
    University of Skövde, School of Life Sciences.
    Rapid activation of JNK/SAPK in LNCaP prostate cancer cells by 1α,25-dihydroxyvitamin D3 is independent of PDIA3 (1,25-MARRS)2008In: Current Topics in Steroid Research, ISSN 0972-4788, Vol. 5, p. 17-24Article in journal (Refereed)
    Abstract [en]

    1α,25-dihydroxyvitamin D3 (1,25D3 ) is a highly potential anti-cancerous agent for prevention and treatment of prostate cancer, the most commonly diagnosed cancer type of males in western countries. A recent study by our laboratory, demonstrates that LNCaP cancer cells treated with 1,25D3, evoked dose-dependent activation of the JNK/SAPK MAPK signaling pathway within 10 minutes after hormone treatment, indicative of membrane-initiated steroid signaling (MISS) by 1,25D3. This confirms previous reports on intestinal-, chondrocyte- and osteoblast cells, where 1,25D3 operates through pharmacologically distinct nuclear-initiated mechanisms (NISS) and plasma membrane-initiated mechanisms. NISS is mediated via the vitamin D receptor (nVDR) and MISS is mediated through 1,25D3-MARRS (PDIA3, 1,25D3-membraneassociated rapid response steroid binding protein) or nVDR. The aims of the present study were to investigate the mechanisms of MISS evoked effects on alkaline phosphatase (ALP) and activation of the JNK/SAPK by 1,25D3, and the involvement of PDIA3 in 1,25D3 initiated activation of the JNK/SAPK signaling pathway. Furthermore, 1,25D3-treated LNCaP cells were transfected with siRNA against PDIA3 and phosphorylated JNK/SAPK was estimated by western analysis. Western analysis and ALP-assays demonstrated rapid activation of both JNK/SAPK as well as ALP. Silencing of PDIA3 did not affect 1,25D3 mediated activation of JNK/SAPK, suggesting that PDIA3 is not involved in the 1,25D3-initiated activation of the JNK/SAPK signaling pathway.

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