Dysfunction within the mitogen-activated protein kinase (MAPK) cascade has been recognised as a pathological feature of schizophrenia, however the possible mechanistic connection to the disease phenotype remains unexplored. Using the maternal immune activation (MIA) rat model of schizophrenia, the present study investigated the involvement of prefrontal cortex (PFC) MAPK in sensorimotor gating and adaptive learning deficits via western blot, pre-pulse inhibition (PPI) testing, and a contingency degradation operant task, respectively. Principle findings identified a negative relationship between basal MAPK expression and PPI exclusively in MIA rats, suggesting a modulatory role for MAPK in sensorimotor gating pathology. In addition, the correlation between MAPK and adaptive learning capacity observed in control rats was absent for rats exposed to MIA. Findings are considered with respect to the glutamatergic NMDA hypofunction theory of schizophrenia, as well as the critical role of PFC in contingency learning.

丝裂原活化蛋白激酶 (MAPK) 级联反应中的功能障碍已被认为是精神分裂症的病理特征，但与疾病表型的可能机制联系仍未得到探索。本研究使用精神分裂症的母体免疫激活 (MIA) 大鼠模型，通过蛋白质印迹、前脉冲抑制 (PPI) 测试和偶然性退化研究了前额叶皮层 (PFC) MAPK 在感觉运动门控和适应性学习缺陷中的参与操作任务，分别。主要发现确定了基础 MAPK 表达和 PPI 之间的负相关关系，仅在 MIA 大鼠中，表明 MAPK 在感觉运动门控病理学中具有调节作用。此外，对于暴露于 MIA 的大鼠，在对照大鼠中观察到的 MAPK 与适应性学习能力之间没有相关性。研究结果考虑了精神分裂症的谷氨酸能 NMDA 功能减退理论，以及 PFC 在应急学习中的关键作用。