Schizophrenia Research Laboratory, Neuroscience Research Australia, Randwick, NSW, Australia.
School of Psychiatry, University of New South Wales, Sydney, Australia.
Schizophr Bull. 2018 Jun 6;44(4):865-875. doi: 10.1093/schbul/sbx122.
Neuregulin 1 (NRG1) is a schizophrenia candidate gene whose protein product is involved in neuronal migration, survival, and synaptic plasticity via production of specific isoforms. Importantly, NRG1 type III (NRG1 III) mRNA is increased in humans inheriting a schizophrenia risk haplotype for the NRG1 gene (HapICE), and NRG1 protein levels can be elevated in schizophrenia. The nature by which NRG1 type III overexpression results in schizophrenia-like behavior and brain pathology remains unclear, therefore we constructed a transgenic mouse with Nrg1 III overexpression in forebrain neurons (CamKII kinase+). Here, we demonstrate construct validity for this mouse model, as juvenile and adult Nrg1 III transgenic mice exhibit an overexpression of Nrg1 III mRNA and Nrg1 protein in multiple brain regions. Furthermore, Nrg1 III transgenic mice have face validity as they exhibit schizophrenia-relevant behavioral phenotypes including deficits in social preference, impaired fear-associated memory, and reduced prepulse inhibition. Additionally, microarray assay of hippocampal mRNA uncovered transcriptional alterations downstream of Nrg1 III overexpression, including changes in serotonin receptor 2C and angiotensin-converting enzyme. Transgenic mice did not exhibit other schizophrenia-relevant behaviors including hyperactivity, social withdrawal, or an increased vulnerability to the effects of MK-801 malate. Our results indicate that this novel Nrg1 III mouse is valid for modeling potential pathological mechanisms of some schizophrenia-like behaviors, for determining what other neurobiological changes may be downstream of elevated NRG1 III levels and for preclinically testing therapeutic strategies that may be specifically efficacious in patients with the NRG1 (HapICE) risk genotype.
神经调节蛋白 1(NRG1)是精神分裂症的候选基因,其蛋白产物通过产生特定的异构体参与神经元迁移、存活和突触可塑性。重要的是,在继承 NRG1 基因(HapICE)精神分裂症风险单倍型的人类中,NRG1 型 III(NRG1 III)mRNA 增加,并且精神分裂症患者的 NRG1 蛋白水平可以升高。NRG1 型 III 过表达导致类似精神分裂症的行为和脑病理学的性质尚不清楚,因此我们构建了一种在大脑前神经元中过表达 Nrg1 III 的转基因小鼠(CamKII 激酶+)。在这里,我们证明了这种小鼠模型的构建有效性,因为幼年和成年 Nrg1 III 转基因小鼠在多个脑区表现出 Nrg1 III mRNA 和 Nrg1 蛋白的过表达。此外,Nrg1 III 转基因小鼠具有面部有效性,因为它们表现出与精神分裂症相关的行为表型,包括社交偏好缺陷、恐惧相关记忆受损和前脉冲抑制减少。此外,海马 mRNA 的微阵列分析揭示了 Nrg1 III 过表达的下游转录改变,包括 5-羟色胺受体 2C 和血管紧张素转换酶的改变。转基因小鼠没有表现出其他与精神分裂症相关的行为,包括多动、社会回避或对 MK-801 马来酸盐作用的易感性增加。我们的结果表明,这种新型 Nrg1 III 小鼠可有效模拟某些类似精神分裂症行为的潜在病理机制,用于确定升高的 NRG1 III 水平的下游可能发生哪些其他神经生物学变化,并用于临床前测试可能对具有 NRG1(HapICE)风险基因型的患者特别有效的治疗策略。