Dr. Gong Chen, Thesis Supervisor Przemyslaw Maslak, Thesis Honors Advisor
Keywords:
Neuroscience Rett Syndrome Dendritic Spine Morphogenesis GABA
Abstract:
Dendritic spines are critical elements in establishing excitatory synapses in cortical circuits. The alteration of dendritic spines in shape and number is believed to be critical for the refinement of neural circuits and the processing and storage of information within the brain. Neuropathological studies have demonstrated that a number of disease states, ranging from schizophrenia to autism spectrum disorders, display abnormal dendritic spine morphology or distribution. Rett syndrome, a severe form of autism spectrum disorder, is mainly caused by MeCP2 de novo mutations and its mechanism remains to be elucidated. Here we demonstrate that GABA functional deficits may be involved in the aberrant spine plasticity that, in part, underlie the pathophysiology of Rett syndrome. In order to study the mechanistic action of MeCP2 in controlling dendritic spine morphogenesis, the use of cultured mouse cortical neurons was employed. Our data suggests that GABA function may serve as an alternative therapeutic approach for the treatment of Rett syndrome.
