Larson, Abigail K2018-04-122018-04-122018-04-12https://hdl.handle.net/11299/195691The purpose of this study was to determine how retinoic acid (RA) signaling affects the maturation of paravalbumin (PV) interneurons in the postnatal prefrontal cortex (PFC). RA plays an important role in early development of the brain and abnormal RA signaling has been associated with schizophrenia, depression and bipolar disorders. Due to the important role RA plays in the brain, the Nakagawa Lab has been studying the roles RA signaling plays in the development of interneurons in the PFC, which are important regulators of excitation-inhibition balance and synchronous firing which forms the basis of our cognition and emotion. We have found that in mice that are deficient of the Cyp26b1 gene, which encodes a RA-degrading enzyme, the number of a subtype of interneurons, called PV interneurons, is increased in postnatal PFC but there is a non-significant difference in survival, indicating that in normal brains RA may promote the maturation of PV interneurons. The goal of my research project is to determine how PV maturation differs in mice with excessive RA signaling, i.e., Cyp26b1 mutant mice. An increase in the number of PV neurons surrounded by perineuronal nets will indicate accelerated maturation. It’s been shown that the number of cells that express PV mRNA is increased in mutant mice at P14 and P21 and the protein is also increased at P14 in the mutants. Therefore, I first focused on these stages and compared the number of PV neurons and perineuronal net positive cells between the Cyp26b1 knockout mice and control littermates.enPresentation