| Summary: | 碩士 === 國立臺灣大學 === 解剖學暨細胞生物學研究所 === 101 === Maternal infection during pregnancy is a noticed risk factor for neurodevelopment psychiatric disorders, such as schizophrenia and autism. Accumulating evidence suggests that adverse life experiences such as social isolation have been associated with the onset of psychosis. Therefore, our study aimed to test whether prenatal infection could interact with postweaning social isolation to induce behavioral deficits and neuronal alterations in the mesocortical dopamine system. In the present study, we treated the pregnant mice of C57BL/6 background with a single injection of polyriboinosinic: polyribocytidilic acid (Poly I:C, 20 mg/kg, i.p.) at gestation day 9 to mimic prenatal infection. After weaning at postnatal day P30, male offspring were reared individually to mimic social isolation or in group (3-5). Phenotypes were characterized in various aspects after P60. In the behavioral aspect, only poly I:C-offspring exhibited hypolocomotor activity in a novel open field but not in isolated-mice. Notably, impairment of short-term memory function tested in novel-object recognition task and prepulse inhibition deficits were found in all experiment groups compared to the control group. The number of dopaminergic neurons in the ventral tegmental area (VTA) was increased in poly I:C-offspring whereas the number of parvalbumin-expressing neurons in the medial prefrontal cortex (mPFC) was decreased in isolated-offspring. Histologically, the dendritic architecture of the layer II/III pyramidal neurons in the mPFC was examined. Alterations in dendritic complexity and reduced spine density were present in all experiment groups. Together, our data demonstrated that prenatal infection combined with postweaning social isolation lead to cognitive deficits and neuronal alteration, thus, it could be a model for neurodevelopment psychiatric disorders.
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