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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 103 (1996), S. 947-955 
    ISSN: 1435-1463
    Keywords: Serotonin ; interferon ; wet-dog shake ; opioid receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acute (1h) intraperitoneal (ip) treatment with interferon (IFN)-α-2a (300IU/g) significantly inhibited wet-dog shakes (WDS) induced by (±)-1-(2,5-dimethoxy-4-iodophenyl)-2 aminopropane (DOI; 0.5, 1.0mg/kg), which is mediated by serotonin (5-hydroxytryptamine; 5-HT)2 receptor in rats. IFN-α did not affect spontaneous locomotion. The inhibition of DOI (0.5mg/kg)-induced WDS by IFN-α was dose (90–300 IU/g)- and time (1–6 h)-dependent, and was prevented by 30 min pretreatment with naltrexone (NLTX; 1.0mg/kg, ip), an opioid receptor antagonist. Acute (1h) intracerebroventricular (icv) treatment with IFN-α (1,500IU/rat) also inhibited DOI (0.5mg/kg)-induced WDS, and the effect was blocked by NLTX (50μg/rat, icv). These results suggest that IFN-α may modulate 5-HT2 receptor-mediated behavior through opioid receptors in the central nervous system.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    ISSN: 1435-1463
    Keywords: Serotonin2 receptor ; α2-adrenergic receptor ; calcium mobilization ; heterologous supersensitization ; human platelets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent reports suggest that serotonin (5-HT)2 receptor-mediated second messenger systems are enhanced in platelets of affective disorders. To make the mechanism of the enhanced response clear, we investigated 5-HT2 and alpha (α)2-adrenergic receptor-induced intracellular calcium (Ca2+) mobilization in platelets of healthy volunteers, using fura-2. 5-HT2 and α2-adrenergic receptor-mediated Ca2+ mobilization was enhanced by prior exposure to the other type of agonist, so called “heterologous supersensitization”. The supersensitization was due to the enhancement of maximal response without change in agonist affinity. Chelating extracellular Ca2+ did not diminish the supersensitization. This enhancement of Ca2+ mobilization was not inhibited by H-7, an inhibitor of protein kinase C. However, this supersensitization was inhibited by pretreatment with sodium fluoride which directly activates guanine nucleotide binding regulatory proteins (G proteins). These results suggest that the supersensitization was caused from intracellular Ca2+ storage sites through a G protein-coupled pathway.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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