| 1 | 摩尔。细胞。生物。2005年5月25日：4221-8 |
|---|---|
| PMID | 15870291 |
| 标题 | RGS4突变小鼠的产生和表征。 |
| Abstract | RGS蛋白是通过异三聚体G蛋白偶联受体的信号传导的负调节剂，因此，可以调节过多的生物学现象。但是，这些刚刚开始在体内探索。在这里，我们描述了RGS4缺陷的小鼠线，这是一个通常在分化神经元的离散群体中，后来在中枢神经系统的多个位点上，尤其是皮层的基因，尤其是它是最高度转录的RGS之一。基因。RGS4（LACZ/LACZ）小鼠具有正常的神经发育，并且可行且肥沃。突变成人的行为测试揭示了微妙的感觉运动缺陷schizophreniasusceptibility gene (by showing intact prepulse inhibition in the mutants) nor (unlike another member of the Rgs family,RGS9) a role of Rgs4 in the acute or chronic response to opioids. |
| SCZ关键字 | schizophrenia, schizophrenic |
| 2 | Synapse 2006 Sep 60: 319-46 |
| PMID | 16786561 |
| 标题 | 精神病路径收敛通过D2high多巴mine receptors. |
| Abstract | 这篇综述的目的是确定神经化学敏感性改变的靶标或生物标志物，这是许多与街头药物，脑损伤，类固醇使用，出生损伤和基因改变相关的人类精神病模型共有的。人类的精神病可能是由苯丙胺，苯二肽，类固醇，乙醇和脑部病变（如海马，皮质和内嗅病变）引起的。令人惊讶的是，大鼠中的所有这些药物和病变都会导致多巴胺超敏反应，并在striata中增加200-400％的多巴胺D2受体或D2HIGH的高亲和力状态。在剖腹产和用皮质酮或抗精神病药治疗的大鼠中，发生类似的超敏反应和D2高升高发生在大鼠中，例如抗精神病药，利培酮，利培酮，氟哌啶醇，奥氮平，奥氮平，quetiapine和clozapine，其诱导D2HIGH高度均小于haloper或haloper haloper或cliozapine。奥氮平。有一些可能的基因淘汰的老鼠schizophrenia敏感性基因是多巴胺超敏感的，其纹状体揭示了D2高态的升高。这些基因包括多巴胺β-羟化酶，多巴胺D4受体，G蛋白受体激酶6，酪氨酸羟化酶，儿茶酚-O-甲基转移酶，痕量胺1受体，G蛋白信号传导的调节剂RGS9, and the RIIbeta form of cAMP-dependent protein kinase (PKA). Striata from mice that are not dopamine supersensitive did not reveal elevated D2High states; these include mice with knockouts of adenosine A2A receptors, glycogen synthase kinase GSK3beta, metabotropic glutamate receptor 5, dopamine D1 or D3 receptors, histamine H1, H2, or H3 receptors, and rats treated with ketanserin or aD1 antagonist. The evidence suggests that there are multiple pathways that convergetoelevate the D2High state in brain regions and that this elevation may elicit psychosis. This proposition is supported by the dopamine supersensitivity that is a common feature ofschizophreniaand that also occurs in many types of genetically altered, drug-altered, and lesion-altered animals. Dopamine supersensitivity, in turn, correlates with D2High states. The finding that all antipsychotics, traditional and recent ones, act on D2High dopamine receptors further supports the proposition. |
| SCZ关键字 | schizophrenia, schizophrenic |
| 3 | Synapse 2007 5月61日：303-9 |
| PMID | 17318883 |
| 标题 | Consistent with dopamine supersensitivity, RGS9 expression is diminished in the amphetamine-treated animal model of schizophrenia and in postmortem schizophrenia brain. |
| Abstract | It is known thatRGS9-2基因基因敲除小鼠对DA表现出超敏反应，并且在DA（D2（高）受体）的高亲和力状态下DA D2受体的比例显着升高。因为这与来自具有schizophrenia，我们检查了来自患有疾病和脑纹状体的受试者的尸体中枢神经系统组织是否是精神病动物模型或schizophrenia（苯丙胺敏感大鼠）的水平改变了RGS9-2。mRNARGS929个对照海马中的-2为0.185 +/- 0.015 fg，每FBβ-葡萄糖醛酸酶mRNA（平均+/- SE），而29schizophreniahippocampi was 0.145 +/- 0.015 fg per fg of beta-glucuronidase mRNA (average +/- SE), a reduction of 22%. Of the many receptor-regulating genes related to G proteins, and of 11 RGS genes,RGS9-2是苯丙胺敏化大鼠纹状体中最多的。降低的水平RGS9-2 expression in both an animal model ofschizophreniaand a postmortemschizophreniabrain provide further evidence implicatingRGS9-2作为候选基因schizophrenia. |
| SCZ关键字 | schizophrenia, schizophrenic |
| 4 | 是。J. Med。基因。B Neuropsychiatr。基因。2009年3月150B：239-42 |
| PMID | 18548510 |
| 标题 | Analysis of genetic variations in the RGS9 gene and antipsychotic-induced tardive dyskinesia in schizophrenia. |
| Abstract | 一些患者患有抗精神病药长期治疗的患者会出现迟发性运动障碍（TD），这是一种异常的非自愿运动障碍。典型的抗精神病药D（2）多巴胺受体（D（2）DR）并产生D（2）DR Supersenitivity。相反，G蛋白信号传导（RGS）的调节剂可以增强G蛋白偶联D（2）DR的信号终止。此外，在长期抑制多巴胺能传播后，多巴胺能激动剂仅在RGS9敲除小鼠，但不在正常小鼠中。因此，人类的变化RGS9gene may be related to susceptibility to TD. In this study,schizophrenicinpatients receiving long-term antipsychotic treatment were assessed using the Abnormal Involuntary Movement Scale twice over a 3-month interval. Only patients in whom abnormal involuntary movements were absent (non-TD group) and those who showed persistent TD (TD group) were enrolled. There were 407 patients in the study sample (TD = 252; non-TD = 155) and seven single nucleus polymorphisms (SNPs) in theRGS9为每个受试者均基因分型。在这项研究中，TD组和非TD组之间的基因型和等位基因分布没有差异，但与RS4790953的等位基因关联趋势较弱（P = 0.0399）。在单倍型分析中，AGG单倍型（RS8077696-RS8070231-RS2292593）的显着关联RGS9gene was found (permutation P = 0.007), and this is worthy of replication and further study. |
| SCZ关键字 | schizophrenia, schizophrenic |
| 5 | 是。J. Med。基因。B Neuropsychiatr。基因。2009年3月150B：239-42 |
| PMID | 18548510 |
| 标题 | Analysis of genetic variations in the RGS9 gene and antipsychotic-induced tardive dyskinesia in schizophrenia. |
| Abstract | 一些患者患有抗精神病药长期治疗的患者会出现迟发性运动障碍（TD），这是一种异常的非自愿运动障碍。典型的抗精神病药D（2）多巴胺受体（D（2）DR）并产生D（2）DR Supersenitivity。相反，G蛋白信号传导（RGS）的调节剂可以增强G蛋白偶联D（2）DR的信号终止。此外，在长期抑制多巴胺能传播后，多巴胺能激动剂仅在RGS9敲除小鼠，但不在正常小鼠中。因此，人类的变化RGS9gene may be related to susceptibility to TD. In this study,schizophrenicinpatients receiving long-term antipsychotic treatment were assessed using the Abnormal Involuntary Movement Scale twice over a 3-month interval. Only patients in whom abnormal involuntary movements were absent (non-TD group) and those who showed persistent TD (TD group) were enrolled. There were 407 patients in the study sample (TD = 252; non-TD = 155) and seven single nucleus polymorphisms (SNPs) in theRGS9为每个受试者均基因分型。在这项研究中，TD组和非TD组之间的基因型和等位基因分布没有差异，但与RS4790953的等位基因关联趋势较弱（P = 0.0399）。在单倍型分析中，AGG单倍型（RS8077696-RS8070231-RS2292593）的显着关联RGS9gene was found (permutation P = 0.007), and this is worthy of replication and further study. |
| SCZ关键字 | schizophrenia, schizophrenic |
| 6 | Psychiatr. Genet. 2010 Feb 20: 47-8 |
| PMID | 20016399 |
| 标题 | G蛋白信号9（RGS9）的调节剂与犹太人口中的精神分裂症之间没有关联。 |
| Abstract | -1 |
| SCZ关键字 | schizophrenia, schizophrenic |
| 7 | J. Neurochem. 2010 Aug 114: 739-49 |
| PMID | 20477943 |
| 标题 | RGS9-2 mediates specific inhibition of agonist-induced internalization of D2-dopamine receptors. |
| Abstract | Regulator of G protein signaling 9-2 (RGS9-2), a member of the RGS family of GTPase accelerating proteins, is expressed specifically in the striatum, a brain region involved in controlling movement, motivation, mood and addiction.RGS9可以在中刺纹状体神经元中与D（2） - 类多巴胺受体共定位-2，并改变两者的功能RGS9-2和D（2）类似多巴胺受体已与schizophrenia, movement disorders and reward responses. Previously we showed thatRGS9-2 can specifically co-localize with D(2)-dopamine receptors (D2R). Here we provide further evidence of the specificity ofRGS9-2用于调节D2R细胞函数：表达RGS9-2抑制D2R的多巴胺介导的细胞内在化，而另一种RGS蛋白RGS4的表达无效。此外，激动剂介导的G蛋白偶联三角洲阿片类受体的内在化不受影响RGS9-2 expression. We utilized mutant constructs ofRGS9-2 to show that theRGS9-2 DEP (for Disheveled, EGL-10, Pleckstrin homology) domain and the GTPase accelerating activity ofRGS9-2 were necessary for mediating specific inhibition of D2R internalization. |
| SCZ关键字 | schizophrenia, schizophrenic |
| 8 | Curr Neuropharmacol 2011 Mar 9: 190-4 |
| PMID | 21886588 |
| 标题 | G蛋白信号传导9基因的调节剂与甲基苯丙胺使用障碍和精神分裂症患者之间的关联。 |
| Abstract | G蛋白信号传导（RGS）的调节剂调节异三聚体G蛋白的功能。RGS9-2 is highly expressed in the striatum and plays a role in modulating dopaminergic receptor-mediated signaling cascades. Previous studies suggested that theRGS9基因可能有助于对精神病的易感性。因此，我们调查了RGS9gene and two related dopamine psychoses,schizophreniaand methamphetamine use disorders. The subjects comprised 487 patients ofschizophreniaand 464 age- and sex-matched healthy controls and 220 patients of methamphetamine use disorder and 289 controls. We genotyped two nonsynonymous polymorphisms, rs12452285 (Leu225Ser) and rs34797451 (His498Arg), of theRGS9基因。RS34797451在目前的日本人群中显示出单态，但RS12452285显示出多态性。患者的基因型或等位基因分布没有显着差异schizophreniaand the corresponding control or between patients with methamphetamine use disorder and the corresponding control. We also analyzed the clinical features of methamphetamine use disorder. We found a significant association in allelic distribution with the phenotypes of age at first consumption (p=0.047). The present study suggested that theRGS9基因不太可能在schizophrenia至少在日本人群中，甲基苯丙胺依赖性责任和/或甲基苯丙胺诱导的精神病的发展。 |
| SCZ关键字 | schizophrenia, schizophrenic |
| 9 | 神经化学。res。2016年2月41日：183-92 |
| PMID | 26547196 |
| 标题 | Perinatal Treatments with the Dopamine D2-Receptor Agonist Quinpirole Produces Permanent D2-Receptor Supersensitization: a Model of Schizophrenia. |
| Abstract | 用多巴胺D2受体（D2-R）激动剂对围产期大鼠的每日重复治疗一周或更长时间会产生“启动”式糖的现象，但对D2-R的长期敏化。实际上，每天低至50°g/kg/天的奎因螺旋剂量足以使D2-R敏化。当用奎因螺蛋白在大坝上急性治疗时，尖锐的大鼠是新生儿和青春期，在大坝上表现出增强的饮食/gnaw/gnawing/疗法，这也是水平的运动活性。在3至5周之间，急性奎因螺旋对底漆大鼠的治疗可产生深刻的垂直跳跃，爪子踩踏 - 在对照大鼠中未观察到的行为。在后来，急性奎因螺螺质治疗与增强的打哈欠有关，这是D2-R相关的行为。尽管出生时间附近的D2-R启动时期，但这种长期的D2-R超敏反应被认为是终身的。D2-R超敏性与D2-R的数量或亲和力的增加无关，如大鼠纹状体所评估的那样；D3-R Agonist 7-OH-DPAT也不诱导它。然而，奎因螺洛诱导的D2-R超敏反应与认知缺陷有关，也与脉冲前抑制和神经营养因子的缺陷以及G蛋白信号传导（RGS）的转录剂调节剂的低水平有关RGS9in brain; and acute reversal of these alterations by the antipsychotic agent olanzapine. In sum, rats ontogenetically D2-R supersensitized have face validity, construct validity and predictive ability forschizophrenia. |
| SCZ关键字 | schizophrenia, schizophrenic |