Lisa Monteggia (University of Texas, Southwestern Medical School)
MeCP2 dependent regulation of synaptic transmission and complex behavior

RESEARCH INTERESTS

• Development of Animal Models for Psychiatric Diseases
• Role of Growth Factors in Depression
• Elucidating the Role of MeCP2 in Mediating Autistic-like Behavior (autism)
• Role of Transcriptional Repression in Neurons

RESEARCH OVERVIEW

Our research interests focus on the molecular and cellular basis of neural plasticity as it pertains to psychiatric disorders. One major goal of the lab is to identify and understand the role of neurotrophic growth factors in the adult brain. Alterations in these factors and their intracellular signaling pathways have been suggested to play an important role in many psychiatric illnesses including depression. These neurotrophins, in particular brain-derived neurotrophic factor (BDNF), and their receptors are being studied in conditional and inducible cell-type specific knockout mice, as well as with the use of viral technology, to elucidate their role in neuronal function and complex behavior. As a complementary approach, we are using primary neuronal cultures to elucidate the signaling pathways by which these growth factors may be producing their effects. A second major goal of the lab is to examine the role of transcriptional repression on synaptic function. This project is focused on examining functional alterations that occur in neurons following the loss of synaptic repression. This approach is being coupled with studies examining a specific transcriptional repressor, methyl-CpG-binding protein (MeCP2), that has been linked as the causative factor in the neurodevelopmental disorder, Rett Syndrome. We are currently characterizing MeCP2 knockout mice in a broad array of behavioral paradigms focusing on modeling autistic-like behavior, as well as functionally examining how the loss of MeCP2 contributes to the disease state.

Questions? Want to meet with the speaker?

Contact Anne Andrews, ama11@psu.edu or phone 865-2970