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  • Articles: DFG German National Licenses  (3)
  • 5-HT-2 receptors  (1)
  • 5-HT-2A receptors  (1)
  • Serotonin  (1)
  • 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
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  • 2
    ISSN: 1435-1463
    Keywords: 5-HT-2 receptors ; cGMP generation ; nitric oxide ; desensitization ; C6 glioma cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Serotonin (5-HT)-2 receptor-mediated cGMP generation was investigated in comparison with calcium (Ca2+) mobilization in C6 glioma cells. 5-HT enhanced cGMP generation, and risperidone and ketanserin potently blocked the response. These results indicate that 5-HT-2 receptors are responsible for the cGMP generation. 5-HT-induced cGMP production was completely abolished by BAPTA, an intracellular Ca2+ chelating agent, or N g -monomethyl-L-arginine (NMMA), a nitric oxide synthase (NOS) inhibitor, suggesting that 5-HT-induced cGMP generation was through nitric oxide (NO)-dependent pathway. 5-HT (10 μM)-elicited Ca2+ mobilization and cGMP generation were reduced to 40 and 15 % after pretreatment with 10 μM 5-HT for 4 hours. NMMA did not modify 5-HT-induced desensitization of either Ca2+ mobilization or cGMP generation, suggesting that NO pathway is independent of the desensitization. The present study has demonstrated the nature of 5-HT-2 receptormediated cGMP generation in C6 glioma cells.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-1463
    Keywords: Keywords: Heat shock protein ; calcium ; serotonin ; 5-HT-2A receptors ; quercetin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. This study was conducted to investigate an effect of heat stress at 44°C for 30 min on intracellular Ca2+ signaling system and on heat shock protein (HSP)-70 expression. 5-HT-induced Ca2+ mobilization was reduced 1, 3 and 6 hrs after heat stress, and recovered to the control level 12 and 24 hrs after heat stress. One hr after heat stress, Ca2+ rise was significantly decreased when the cells were stimulated by any concentration of 5-HT. Thrombin-induced Ca2+ increase was also markedly reduced 1 hr after heat stress. HSP-70 level was increased 6 and 9 hr after heat stress. In HSP synthesis inhibitor quercetin-treated cells, HSP-70 expression was not enhanced after heat stress, and Ca2+ rise in response to 5-HT did not return to the control level. However, the Ca2+ rise induced by 5-HT was not restored to the control level after stress in Ac-Asp-Glu-Val-Asp-H (DEVD)-exposed cells while DEVD had little effect on heat stress-induced synthesis of HSP-70. Dexamethasone did not alter the change in HSP-70 expression or Ca2+ response after heat stress. These results indicate that heat stress attenuated 5-HT-induced Ca2+ mobilization and that HSP-70 expression played an important role in recovery from Ca2+ impairment, possibly via protease activity in C6 cells.
    Type of Medium: Electronic Resource
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