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摘要:Dopamine(DA) is critical in mental physiology(rewards, learning and memory) and diseases(depression, addiction, Parkinson’s disease). DA receptor D2 R is a Gi-sensitive GPCR. Strength of membrane depolarization is either dependent on depolarization amplitude/duration under voltage clamp, or action potential(AP) frequency under current clamp. Following field potential pulses at medial forebrain bundle(MFB) to trigger APs in DA neurons, DA release from striatum in vivo is induced and recorded by electrochemical carbon fiber electrode(CFE). The evoke DA overflow was dependent on both number and frequency of APs. D2 R antagonist haloperidol(0.37mg/kg) enhances DA release. Interestingly, the relative enhancement of haloperidol-mediated DA release, g(f), was strongly dependent on AP-frequency. In presence of haloperidol, g(20Hz) > 10*g(80Hz) in wild type mice. The f-dependence was fully abolished in D2-KO mice, indicating D2 R is responsible for the f-dependent g(f). Since AP-frequency is equal to membrane-depolarization strength, we investigate voltage dependence of D2R-Gi(vG i) in cultured Hela cells expressing D2R2. vG i-D2 R was measured by co-expression of D2R-Gаiq-GCa MP3, which shows GCa MP3-reported Ca2+-release from ER in response to activating D2 R. This in-vitro system shows, membrane depolarization reduces D2R-mediated Ca2+ signal, indicating D2R-activation is indeed voltage-dependent. This in-vitro D2R-experiments strongly support the notion that D2R-activity is voltage-dependent in striatum in vivo.
会议名称:

第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

会议时间:

2015-09-20

会议地点:

中国浙江桐乡

  • 专辑:

    基础科学; 医药卫生科技

  • 专题:

    生物学; 基础医学

  • 分类号:

    R338

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