Doris Lam is a neuroscientist specializing in neuroimmunology. Her research interest is in understanding the interaction between different cell types in the central nervous system (CNS). Her research has used multi-disciplinary approaches (electrophysiology, and cell and molecular biology) to identify mechanisms that regulate cellular activity in CNS cells (e.g. neurons and microglia), and how they contribute to neurodegenerative diseases. Lam's current work focuses on reproducing the CNS on an in-vitro, chip-based Human Investigational Platform.
Honors and Awards
- OSOTF Dalton Whitebread Scholarship Fund
- SGS Conference Grant
- ORT Conference Travel Award
- Award winner for Excellence in Poster Presentation, 2015 Collaborative Program in Neuroscience (CPIN) Research Day
- Award winner for Outstanding Poster Presentation, 2013 CPIN Research Day
- University of Toronto Fellowship
- College of Medicine Graduate Scholarship
- Orange Benevolent Society of Saskatchewan
Selected Recent Publications
Lam, D., and Schlichter, L.C. (2015) Expression and contributions of the Kir2.1 inward-rectifier K+ channel to proliferation, migration and chemotaxis of microglia in unstimulated and anti-inflammatory states. Frontiers Cellular Neuroscience, 9:185. doi: 10.3389/fncel.2015.00185.
Schlichter, L.C., Jiang, J., Wang, J., Newell, E.W., Tsui, F.W., and Lam, D. (2014) Regulation of hERG and hEAG channels by Src and by SHP-1 tyrosine phosphatase via an ITIM region in the cyclic nucleotide binding domain. PLoS One, 9(2): e90024. doi: 10.1371/journal.pone.0090024.
Thiele, S., Warre, R., Khademullah, C.S., Fahana, N., Lo, C., Lam, D., Talwar, S., Johnston, T.H., Brotchie, J.M., and Nash, J.E. (2011) Generation of a model of L- DOPA-induced dyskinesia in two different mouse strains. Journal of Neuroscience Methods, 197: 193-208. doi: 10.1016/j.jneumeth.2011.02.012.
Warre, R., Thiele, S., Kamal, M., Johnston, T.H., Wang, S., Lam, D., Lo, C., Khademullah, C.S., Perera, G., Reyes, G., Sun, X.S., Brotchie, J.M., and Nash, J.E. (2011) Altered function of glutamatergic cortico-striatal synapses causes output pathway abnormalities in a chronic model of parkinsonism. Neurobiology of Disease, 41: 591-604. doi: 10.1016/j.nbd.2010.10.013.