Su Mi Park, Ph.D.

Imbalanced inhibitory and excitatory neuronal signals have been implicated in autism, and may lead to functional changes in certain brain areas involved in behavioral regulation. Using combinational experimental approaches such as optogenetics, electrophysiology, animal behavioral tests, and immunohistochemistry, I want to investigate how the changes in the neuronal signals shown in a genetic animal model for autism influence a certain neuronal circuitry leading to a specific behavior characterized in autism, and if it is possible to modulate the behavior by manipulating the level of neuronal activity. I would also like to further examine possible biological and environmental factors that can modulate the neuronal activity similar to the experimental manipulations.

My general topic of research was the neuronal mechanism of certain emotional and cognitive behaviors. My master’s thesis research investigated effects of immune challenge on animals’ palatable food intake and correlated changes in neuronal activity, mainly in the hypothalamus, including orexin-A and CART neurons, nucleus accumbens, and amygdala, based on c-Fos expression. My dissertation work investigated the possible influence of 5-HT3 receptor blockade on fear extinction memory and the level of GABAA receptor changes in the amygdala, medial prefrontal cortex, and hippocampus on the fear extinction training of animals that received 5-HT3 receptor antagonists systemically, which tested whether 5-HT3 receptor blockade influences fear extinction via modulation of GABAergic signal. My postdoctoral work was a multidisciplinary approach for developing novel therapeutic agents for psychiatric disorders. In this collaborative work, I evaluated antipsychotic properties of newly-developed functionally selective dopamine D2 receptor ligands for beta arrestin signaling pathway using pharmacological and genetic mice models of hypoglutamatergia and hyperdopaminergia.

Bridi M, Park S.M., Huang S. Developmental disruption of GABA_AR-meditated inhibition in Cntnap2 KO mice. eNeuro 2017, 4(5): 0162-17. (PMID: 28966979)

Park, S.M., Chen, M., Schmerberg, C.M., Dulman, R.S., Rodriguiz, R.M., Caron, M.G., Jin, J. and Wetsel W.C. (2015). Effects of β-Arrestin Biased Dopamine D2 Receptor Ligands on Schizophrenia-like Behavior in Hypoglutamatergic Mice. Neuropsychopharmacology.http://www.ncbi.nlm.nih.gov/pubmed/26129680

Park, S.M. and Williams, C. L. (2012). Contribution of Serotonin Type 3 Receptors in the Successful Extinction of Cued or Contextual Fear Conditioned Responses: Interactions with GABAergic Signaling. Rev Neurosci, 23, 555-569. http://www.ncbi.nlm.nih.gov/pubmed/23087085

Gaykema, R.P.A., Daniels, T.E., Shapiro, N.J., Thacker, G.C., Park, S.M., Goehler, L.E. (2009). Immune challenge and satiety-related activation of both distinct and overlapping neuronal populations in the brainstem indicate parallel pathways for viscerosensory signaling. Brain Research, 1294, 61-79 http://www.ncbi.nlm.nih.gov/pubmed/19646973

Park, S.M., Gaykema, R.P.A. and Goehler, L.E. (2008). How does immune challenge inhibit ingestion of palatable food? Evidence that systemic lipopolysaccharide treatment modulates key nodal points of feeding neurocircuitry. Brain, Behavior &, Immunity, 22(8), 1160-1172. http://www.ncbi.nlm.nih.gov/pubmed/18562160

Gaykema, R.P.A., Park, S.M., McKibbin, C.R. and Goehler, L.E. (2008). Lipopolysaccharide suppresses activation of the tuberomammillary histaminergic system concomitant with behavior: A novel target of immune-sensory pathways. Neuroscience, 152(1), 273-287 http://www.ncbi.nlm.nih.gov/pubmed/18082968

Goehler, L.E., Park, S.M., Opitz, N., Lyte, M. and Gaykema, R.P.A. (2008). Campylobacter jejuni infection increases anxiety-like behavior in the holeboard: Possible anatomical substrates for viscerosensory modulation of exploratory behavior. Brain, Behavior &, Immunity, 22(3), 354-366. http://www.ncbi.nlm.nih.gov/pubmed/17920243