Santos Camila Mauricio, Peres Fernanda Fiel, Diana Mariana Cepollaro, Justi Veronica, Suiama Mayra Akimi, Santana Marcela Gonçalves, Abílio Vanessa Costhek
LiNC - Interdisciplinary Laboratory of Clinical Neurosciences, Department of Psychiatry, Universidade Federal de São Paulo (UNIFESP), Rua Pedro de Toledo, 669, 3° andar, Ed. de Pesquisas II, CEP 04039-032 São Paulo, SP, Brazil.
LiNC - Interdisciplinary Laboratory of Clinical Neurosciences, Department of Psychiatry, Universidade Federal de São Paulo (UNIFESP), Rua Pedro de Toledo, 669, 3° andar, Ed. de Pesquisas II, CEP 04039-032 São Paulo, SP, Brazil; Department of Pharmacology, Universidade Federal de São Paulo (UNIFESP), Rua Pedro de Toledo, 669, 5° andar, Ed. de Pesquisas II, CEP 04039-032 São Paulo, SP, Brazil.
Schizophr Res. 2016 Oct;176(2-3):552-559. doi: 10.1016/j.schres.2016.06.006. Epub 2016 Jun 21.
Schizophrenia is a highly disabling mental disorder, in which genetics and environmental factors interact culminating in the disease. The treatment of negative symptoms and cognitive deficits with antipsychotics is currently inefficient and is an important field of research. Environmental enrichment (EE) has been suggested to improve some cognitive deficits in animal models of various psychiatric disorders. In this study, we aimed to evaluate a possible beneficial effect of early and long-term exposure to EE on an animal model of schizophrenia, the SHR strain. Young male Wistar rats (control strain) and SHRs (21 post-natal days) were housed for 6weeks in two different conditions: in large cages (10 animals per cage) containing objects of different textures, forms, colors and materials that were changed 3 times/week (EE condition) or in standard cages (5 animals per cage - Control condition). Behavioral evaluations - social interaction (SI), locomotion, prepulse inhibition of startle (PPI) and spontaneous alternation (SA) - were performed 6weeks after the end of EE. SHRs presented deficits in PPI (a sensorimotor impairment), SI (mimicking the negative symptoms) and SA (a working memory deficit), and also hyperlocomotion (modeling the positive symptoms). EE was able to reduce locomotion and increase PPI in both strains, and to prevent the working memory deficit in SHRs. EE also increased the number of neurons in the CA1 and CA3 of the hippocampus. In conclusion, EE can be a potential nonpharmacological strategy to prevent some behavioral deficits associated with schizophrenia.
精神分裂症是一种极具致残性的精神障碍,其中遗传因素和环境因素相互作用最终导致该疾病。目前,使用抗精神病药物治疗阴性症状和认知缺陷的效果不佳,这是一个重要的研究领域。环境富集(EE)已被建议可改善各种精神疾病动物模型中的一些认知缺陷。在本研究中,我们旨在评估早期和长期暴露于EE对精神分裂症动物模型SHR品系的可能有益影响。将年轻雄性Wistar大鼠(对照品系)和SHRs(出生后21天)在两种不同条件下饲养6周:置于大笼子(每个笼子10只动物)中,笼子里有不同质地、形状、颜色和材料的物品,每周更换3次(EE条件),或置于标准笼子(每个笼子5只动物 - 对照条件)。在EE结束6周后进行行为评估——社交互动(SI)、运动、惊吓前脉冲抑制(PPI)和自发交替(SA)。SHRs在PPI(一种感觉运动障碍)、SI(模拟阴性症状)和SA(一种工作记忆缺陷)方面存在缺陷,并且还存在运动亢进(模拟阳性症状)。EE能够减少两种品系的运动并增加PPI,并预防SHRs的工作记忆缺陷。EE还增加了海马体CA1和CA3区的神经元数量。总之,EE可能是一种潜在的非药物策略,可预防与精神分裂症相关的一些行为缺陷。