Morgan Bridi, Ph.D.
2015-present Staff Scientist, Hussman Institute for Autism, Baltimore, MD
2015 Ph.D. Neuroscience, University of Pennsylvania, Philadelphia, PA
2009 B.S. Psychology, West Virginia University, Morgantown, WV
2009 B.S. Biology, West Virginia University, Morgantown, WV
Alteration to neuronal connections within and between regions of the brain can have major impacts on neuronal function as well as behavior. Utilizing my experience with both the analysis of behavior and the investigation of the electrophysiological properties of neurons, I will investigate the manipulation of genes involved in the development of neuronal connectivity. I hope that a better understanding of how these genes contribute to neuronal function, and how alterations in those functions impact behavior, will improve our knowledge of the altered brain function found in Autism Spectrum Conditions.
My graduate research focused on the role of epigenetic mechanisms in hippocampus-dependent memory consolidation and hippocampal synaptic plasticity; it involved a combination of behavior, biochemistry, and both field and single-cell electrophysiology in brain slices. My work examined the SIN3A/HDAC complex, which represses transcription by recruiting histone deacetylase enzymes and other histone modifiers to chromatin. I found that loss of SIN3A enhanced hippocampal synaptic potentiation and neuronal excitability, through a mechanism that may involve mGluR5/Homer1 signaling in CA1 pyramidal neurons. I also studied the NR4A family of orphan nuclear receptor transcription factors, a group of acetylation-regulated immediate early genes, and found that their function is critical for transcription-dependent forms of long-term potentiation and the enhancement of potentiation by HDAC inhibitors. Histone modification and the upstream and downstream mechanisms that regulate it have critical roles in both neuronal development and the maintenance of neuronal plasticity. Understanding how these processes regulate plasticity can tell us about the mechanisms of neuronal function, as well as lead to novel therapeutic strategies for neurodegenerative and neurodevelopmental disorders.
Huang S#, Bridi M.S., Kirkwood A#. Dynamic recovery from depression enables rate encoding in inhibitory synapses. 2018. bioRxiv 379081. (#Co-corresponding author)
Bridi M.S., Park SM, Huang S. Developmental disruption of GABAAR-meditated inhibition in Cntnap2 KO mice. eNeuro 2017, 4(5): 0162-17. (PMID: 28966979)
Bridi, M.S.* & Schoch, H.*, Florian, C., Poplawski, S.G., Hawk, J.D., Havekes, R., & Abel, T. The transcriptional co-repressor SIN3A regulates hippocampal synaptic plasticity via Homer1/mGluR5 signaling. (manuscript under revision at the Journal of Clinical Investigation).
Bridi, M.S. & Abel, T. (2013) The NR4A orphan nuclear receptors mediate transcription-dependent hippocampal synaptic plasticity. Neurobiology of Learning and Memory, 105: 151-158.
Bridi, M.S. & Abel, T. (2013) Histone Modifications in the Nervous System and Neuropsychiatric Disorders. In Sweatt, J.D., Meaney, M.J., Nestler, E.J., & Akbarian, S. (Eds.), Epigenetic Regulation in the Nervous System (pp. 35-67). Amsterdam, Netherlands: Elsevier
Hawk, J. D., Bookout, A. L., Poplawski, S. G., Bridi, M., Rao, A. J., Sulewski, M. E., Kroener, B. T., Mangelsdorf, D. J., & Abel, T. (2012). Nr4a nuclear receptors support memory enhancement by histone deacetylase inhibitors. Journal of Clinical Investigation; doi:10.1172/JCI64145