Project: Severe developmental mental disorders such as schizophrenia, bipolar disorder, and autism are leading contributors to cognitive illness, imposing emotional burdens on families as well as individuals. Based on recent literature and our own unpublished data, we hypothesize that postnatal inflammation - and associated proinflammatory mediators - can lead to abnormal activation of astrocytic protein-coupled receptors (GPCRs), which may trigger transmitter and inflammatory mediator release from astrocytes. Both of these effects could consequently alter synaptic transmission during postnatal brain development, and contribute to abnormal long-term changes of excitatory synaptic transmission and plasticity, and thus to changes in sensory processing and the pathogenesis of neuropsychiatric disorders. We propose to directly test this hypothesis using the rodent visual cortex as a model system, chemogenetics, in vivo electrophysiology, behavioral tests for measuring visual memory, and biochemistry. Furthermore, this project will be coupled to a translational project studying Human visual memory as a potential biomarker of developmental mental disorders and using EEG and aye movement recordings. The Master 1 student interested to join our laboratory will contribute to this ambitious projects using one or two of these techniques in mouse models or Human.