作者: Lena Wischhof , Ellen Irrsack , Frank Dietz , Michael Koch
DOI: 10.1016/J.NEUROPHARM.2015.05.029
关键词:
摘要: Maternal infection during pregnancy increases the risk for offspring to develop schizophrenia. However, it is still not fully understood which biochemical mechanisms are responsible emergence of neuropsychiatric symptoms following prenatal immune activation. The serotonin (5-hydroxytryptamine, 5-HT) and glutamate system have prominently been associated with schizophrenia pathophysiology but also mechanism antipsychotic drug actions. Here, we investigated behavioral cellular response 5-HT2A metabotropic (mGlu)2/3 receptor stimulation in male female born lipopolysaccharide (LPS)-treated mothers. Additionally, assessed protein expression levels prefrontal mGlu2 receptors. Prenatally LPS-exposed showed locomotor hyperactivity increased head-twitch behavior agonist DOI. In offspring, mGlu2/3 LY379268 failed reduce DOI-induced prepulse inhibition deficits. LPS-males, changes were further accompanied by enhanced c-Fos an up-regulation No either or found offspring. Our data support hypothesis involvement maternal contributing, at least partially, pathology Identifying alterations that parallel deficits may help improve therapeutic strategies treatment this mental illness. Since most studies rodents almost exclusively include subjects, our contribute elucidating possible gender differences effects on function.