Poster Session 2 - B18
1Anlong Jiang, 1,2,3Fang Liu
1 Department of Physiology, University of Toronto; 2 Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health; 3 Department of Psychiatry, Faculty of Medicine, University of Toronto
Multiple sclerosis (MS) is known as an autoimmune, inflammatory neurological disorder in the central nervous system (CNS) and it affects approximately 2.3 million of people worldwide. The exact etiology of the disease is still not well-defined. Nevertheless, emerging evidence suggests that the MS might be a neurodegenerative disease caused by the glutamate excitotoxicity in the CNS. Using the animal model of MS, the experimental autoimmune encephalomyelitis (EAE) in mice, we have uncovered the expressions of some proteins that are the major components in synaptic vesicle as well as receptor trafficking and regulation have changed. Syntaxin 1B that is involved in the exocytosis, adaptor protein 2 which is a mediator of endocytosis, and Synapsin IIb, a protein that regulates the vesicle pool. Hence, we hypothesize that the mechanism of glutamate vesicle trafficking might be altered in the MS. As the disorder has wide ranges of impacts in the CNS, we picked four critical regions of the brain for examination, cortex, hippocampus, striatum as well as the spinal cord. In the four different regions, the expressions of those proteins vary compared to the controls. Thus, the alternation of the vesicle trafficking system in MS requires further sophisticated investigation and it might be a potential therapeutic target to treat MS.