Student Presenter(s): Himani Jani, Yamini Nori, Jeet Vaishnav
Faculty Mentor: Randy F. Stout, Jr.
Department: Biomedical Sciences
School/College: College of Arts and Sciences, Long Island

Myelin is a specialized cell membrane wrapping that speeds communications between neurons in the nervous system, supports the axons of neurons, and modulates information processing. Gap junctions are protein channels that connect cells of the brain such as the oligodendrocytes which produce myelin. Myelin is lost in diseases such as multiple sclerosis and also in humans carrying certain mutations to gap junction encoding genes. Studies in humans and mice indicate that gap junction connections between astrocytes and oligodendrocytes are required for normal myelin. We hypothesized that the structure of myelin in the cortex (layers 1 and 2) of mice that express a mutant form of Connexin 43 with most of the posttranslationally modified regulatory region deleted would have decreased myelin density and average fiber length due to decreased gap junction communication between astrocytes and oligodendrocytes. We tested this hypothesis by humanely sacrificing mice with mutant and wild-type Connexin 43 (Cx43, aka GJA1) and used immunostaining to label myelin. We used structured illumination microscopy to acquire 3D multi-color channel images of the myelin structure and gap junction expression-localization the mouse brain tissue. We quantified the density and average fiber length of myelin in the two experimental groups (WT and truncation-mutant Cx43 mice). We will present the comparisons of the two groups. Preliminary results indicate the opposite of the expected results-more myelin in.