Mounira Banasr, PhD.

Mounira Banasr, PhD. Assistant Professor, Department of Pharmacology and Toxicology, University of Toronto

Independent Scientist, Campell Family Mental Health Research Institute of CAMH
250 College Street
Toronto, ON M5T 1R8
(416) 535-8501, ext 32319
mounira.banasr@camh.ca

 

Dr. Mounira Banasr received her PhD in Neuroscience from the University of Sciences of Luminy, France in 2004. She went on to complete her post-doctoral fellowship at Yale in one of the top Psychiatry Department in the world, in the laboratory of Ronald Duman, where she became a Junior Scientist in 2008. Dr. Mounira Banasr comes to University of Toronto with extensive experience in mechanisms of depression, stress-related illnesses and novel antidepressants.  She contributed seminal work in these fields, including 1) demonstrating in rodent that astroglial dysfunction participate to the expression of depressive-like behaviors and can be targeted for antidepressant treatment, 2) identifying similar synaptic loss and dysfunction in both human depression and chronic stress rodent models and 3) elucidating the cellular and molecular substrates involved in the rapid antidepressant response of ketamine-like drugs. Dr. Mounira Banasr uses cutting-edge viral and genetic tools to establish a causal link between region-specific and/or cell-specific changes in target genes or molecules and behavioral outcomes in paradigms relevant to multiple psychiatric disorders including depression. Dr Banasr’s research relies on highly translational topics and approaches and combines postmortem studies and chronic stress models to validate the relevance of specific cellular changes in the etiology and for the treatment of major depressive disorder. Her primary interest resides in the investigation of the key molecules, cells and pathways implicated in the expression of the symptoms of depression. Her work focuses on the most consistent findings from human post-mortem studies in depression, the GABAergic, synaptic and astroglial dysfunctions associated with this disorder, and their involvement in the expression of depressive-like behaviors and cognitive impairment. She anticipates that this approach will provide new therapeutic leads for the development of more selective and efficient drugs for the treatment of depression, specifically that targeting these cellular pathologies is a promising new avenue for the development of antidepressant treatments.

Publications:

  1. Chowdhury GM, Zhang J, Thomas M, Banasr M, Ma X, Pittman B, Bristow L, Schaeffer E, Duman RS, Rothman DL, Behar KL, Sanacora G. Transiently increased glutamate cycling in rat PFC is associated with rapid onset of antidepressant-like effects. Mol Psychiatry. 2016 Apr 12. ). Impact factor: 14.4 -
  2. Licznerski, P., Duric, V., Banasr, M., Alavian, K.N., Ota, K.T., Kang, H.J., Jonas, E.A., Ursano, R., Krystal J.H., Duman, R.S. Traumatic Stress Brain Study Group. Decreased SGK1 Expression and Function Contributes to Behavioral Deficits Induced by Traumatic Stress. PLoS Biol. 2015 Oct 27;13(10). Impact factor: 11.7 –
  3. Xu, M., Kobets, A., Du, J.C., Lennington, J., Li, L., Banasr, M., Duman, R.S., Vaccarino, F.M., DiLeone, R.J., Pittenger, C. Targeted ablation of cholinergic interneurons in the dorsolateral striatum produces behavioral manifestations of Tourette syndrome. Proc Natl Acad Sci U S A (PNAS). 2015 Jan 20;112(3):893-8. Impact factor: 10.5 –
  4. Lepack, A.E., Fuchikami, M., Dwyer, J.M., Banasr, M., Duman, R.S. 2014. BDNF release is required for the behavioral actions of ketamine. Int J Neuropsychopharmacol. 2014 Oct 31;18(1). Impact factor: 5.2 –
  5. Voleti, B., Navarria, A., Liu, R.J., Banasr, M., Li, N., Terwilliger, R., Sanacora, G., Eid, T., Aghajanian, G., Duman, R.S., 2013. Scopolamine rapidly increases mammalian target of rapamycin complex 1 signaling, synaptogenesis, and antidepressant behavioral responses. Biological psychiatry 74, 742-749. Impact factor: 5.2 –
  6. Son, H., Banasr, M., Choi, M., Chae, S.Y., Licznerski, P., Lee, B., Voleti, B., Li, N., Lepack, A., Fournier, N.M., Lee, K.R., Lee, I.Y., Kim, J., Kim, J.H., Kim, Y.H., Jung, S.J., Duman, R.S., 2012. Neuritin produces antidepressant actions and blocks the neuronal and behavioral deficits caused by chronic stress. PNAS 109, 11378-11383. Impact factor: 10.5 –
  7. Kang, H.J., Voleti, B., Hajszan, T., Rajkowska, G., Stockmeier, C.A., Licznerski, P., Lepack, A., Majik, M.S., Jeong, L.S., Banasr, M., Son, H., Duman, R.S., 2012. Decreased expression of synapse-related genes and loss of synapses in major depressive disorder. Nature medicine 18, 1413-1417. Impact factor: 28.05 –
  8. Li, N., Liu, R.J., Dwyer, J.M., Banasr, M., Lee, B., Son, H., Li, X.Y., Aghajanian, G., Duman, R.S., 2011. Glutamate N-methyl-D-aspartate receptor antagonists rapidly reverse behavioral and synaptic deficits caused by chronic stress exposure. Biological psychiatry 69, 754-761. Impact factor: 9.4 –
  9. Li, N., Lee, B., Liu, R.J., Banasr, M., Dwyer, J.M., Iwata, M., Li, X.Y., Aghajanian, G., Duman, R.S., 2010. mTOR-dependent synapse formation underlies the rapid antidepressant effects of NMDA antagonists. Science 329, 959-964. Impact factor: 31.48 –
  10. Duric, V., Banasr, M., Licznerski, P., Schmidt, H.D., Stockmeier, C.A., Simen, A.A., Newton, S.S., Duman, R.S., 2010. A negative regulator of MAP kinase causes depressive behavior. Nature medicine 16, 1328-1332. Impact factor: 28.05 –.
  11. Banasr, M., Chowdhury, G.M., Terwilliger, R., Newton, S.S., Duman, R.S., Behar, K.L., Sanacora, G., 2010. Glial pathology in an animal model of depression: reversal of stress-induced cellular, metabolic and behavioral deficits by the glutamate-modulating drug riluzole. Molecular psychiatry 15, 501-511. Impact factor: 15.14 –
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