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摘要:Dopamine(DA) is critical in mental physiology(rewards, learning and memory) and diseases(depression, addiction, PD). DA receptor D2 R is a Gi-sensitive GPCR. Strength of membrane depolarization is either dependent on depolarization amplitude/duration, or action potential(AP) frequency(Artalejo et al., 1992). Following electric pulses at medial forebrain bundle to trigger APs in DA neurons, DA release from striatum is recorded by electrochemical carbon fiber electrode(CFE) in vivo. D2 R blocker haloperidol(0.37mg/kg) enhances AP-induced DA overflow. Interestingly, the relative haloperidol enhancement, ?(f), was strongly dependent on AP-frequency: ?(20Hz) > 10*?(80Hz) in WT-mice. The f-dependence was abolished in D2R-KO mice, indicating D2 R is responsible for the f-dependence of ?(f). This implicated that D2 R is voltage dependent, because AP-frequency is equivalent to membrane-depolarization strength. Thus, we examined voltage dependence of D2R-Gi(vG i) in cultured Hela cells expressing D2R2. vG i-D2 R was measured by co-expression of D2R-G?iq-GCa MP3, as GCa MP3 reported Ca2+-release from ER following activating D2 R. This in-vitro system showed, depolarization significantly inhibited D2R-mediated Ca2+ signal, indicating D2R-activation is indeed sensitive to voltage per se. We thus conclude that membrane-depolarization per se can regulate D2 R and D2R-dependent DA-release 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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