Dickerson Desiree D, Bilkey David K
IST Austria Klosterneuburg, Austria.
Department of Psychology, University of Otago Dunedin, New Zealand.
Front Behav Neurosci. 2013 Dec 27;7:217. doi: 10.3389/fnbeh.2013.00217.
Maternal exposure to infection occurring mid-gestation produces a three-fold increase in the risk of schizophrenia in the offspring. The critical initiating factor appears to be the maternal immune activation (MIA) that follows infection. This process can be induced in rodents by exposure of pregnant dams to the viral mimic Poly I:C, which triggers an immune response that results in structural, functional, behavioral, and electrophysiological phenotypes in the adult offspring that model those seen in schizophrenia. We used this model to explore the role of synchronization in brain neural networks, a process thought to be dysfunctional in schizophrenia and previously associated with positive, negative, and cognitive symptoms of schizophrenia. Exposure of pregnant dams to Poly I:C on GD15 produced an impairment in long-range neural synchrony in adult offspring between two regions implicated in schizophrenia pathology; the hippocampus and the medial prefrontal cortex (mPFC). This reduction in synchrony was ameliorated by acute doses of the antipsychotic clozapine. MIA animals have previously been shown to have impaired pre-pulse inhibition (PPI), a gold-standard measure of schizophrenia-like deficits in animal models. Our data showed that deficits in synchrony were positively correlated with the impairments in PPI. Subsequent analysis of LFP activity during the PPI response also showed that reduced coupling between the mPFC and the hippocampus following processing of the pre-pulse was associated with reduced PPI. The ability of the MIA intervention to model neurodevelopmental aspects of schizophrenia pathology provides a useful platform from which to investigate the ontogeny of aberrant synchronous processes. Further, the way in which the model expresses translatable deficits such as aberrant synchrony and reduced PPI will allow researchers to explore novel intervention strategies targeted to these changes.
孕期中期母亲感染会使后代患精神分裂症的风险增加两倍。关键的起始因素似乎是感染后出现的母体免疫激活(MIA)。在啮齿动物中,通过给怀孕的母鼠注射病毒模拟物聚肌胞苷酸(Poly I:C)可诱导这一过程,它会引发免疫反应,导致成年后代出现结构、功能、行为和电生理表型,这些表型可模拟精神分裂症患者的表现。我们利用这个模型来探究同步在脑神经网络中的作用,这一过程被认为在精神分裂症中存在功能障碍,且先前与精神分裂症的阳性、阴性和认知症状有关。在妊娠第15天给怀孕母鼠注射Poly I:C,会导致成年后代中与精神分裂症病理相关的两个脑区——海马体和内侧前额叶皮质(mPFC)之间的长程神经同步受损。抗精神病药物氯氮平的急性剂量可改善这种同步性降低的情况。先前已证明,MIA动物存在前脉冲抑制(PPI)受损的情况,这是动物模型中精神分裂症样缺陷的金标准测量指标。我们的数据表明,同步性缺陷与PPI受损呈正相关。对PPI反应期间的局部场电位(LFP)活动进行的后续分析还表明,前脉冲处理后mPFC与海马体之间的耦合减少与PPI降低有关。MIA干预能够模拟精神分裂症病理的神经发育方面,这为研究异常同步过程的个体发生提供了一个有用的平台。此外,该模型表达可转化缺陷(如异常同步和PPI降低)的方式,将使研究人员能够探索针对这些变化的新型干预策略。