Abstract

Mitochondria are essential for neuronal function; they provide energy (ATP) to maintain ionic gradients and support synaptic function, and participate in Ca2+ buffering. The complex morphology of neurons presents a unique challenge for mitochondria. Axons and dendrites are long and highly branched, and mitochondria must traffic from the soma and distribute throughout these projections to reach sites of demand. In dendrites, stationary mitochondria localize to sites of high energy consumption and Ca2+ signaling, including synapses and branch points. To understand how these distribution patterns arise during dendritic development, we analyzed the trafficking of mitochondria in dendrites of ganglion cells (GCs) in the intact developing mouse retina. Genetic mutations that disrupt mitochondrial distribution through dendritic branches underlie many common neuropathies, including Dominant Optic Atrophy (DOA). Understanding the mechanisms and functional significance of mitochondrial distribution in neurons is essential for the understanding and treatment of these diseases. We examined mitochondrial distribution and function in a mouse model of DOA to understand how mitochondrial defects give rise to neural pathologies.

Committee Chair

Daniel Kerschensteiner

Committee Members

James Skeath, Aaron Diantonio, Kelly Monk, Valeria Cavalli,

Comments

Permanent URL: https://doi.org/10.7936/K7G15Z46

Degree

Doctor of Philosophy (PhD)

Author's Department

Biology & Biomedical Sciences (Developmental, Regenerative, & Stem Cell Biology)

Author's School

Graduate School of Arts and Sciences

Document Type

Dissertation

Date of Award

Spring 5-15-2016

Language

English (en)

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Available for download on Friday, May 15, 2116

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Biology Commons

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