| Description |
Within the brain, astrocytes provide support and influence the excitability of neurons by regulating the extracellular levels of potassium (K+) and glutamate. These glial cells play a vital role in neural homeostasis by regulating the concentration of neurotransmitters at the synapse, therefore modulating the duration of action potentials. The energy necessary for these mechanisms is supplied by the many mitochondria throughout the astrocyte. Mitochondria within these cells migrate to areas of high demand in order to supply the energy needed to maintain homeostasis. However, the relationship between mitochondrial motility and astrocyte function is poorly understood. The Wilcox lab, in collaboration with the Shaw lab in biochemistry, looks to uncover how the migration of mitochondria within the cell affects the functioning of astrocytes. To understand this issue, astrocytes have been generated that lack Mitochondrial Rho GTPase (Miro1). This protein allows for the proper migration of mitochondria to the cell processes. The Shaw lab has determined that in vitro, the knockout of this protein causes mitochondria to aggregate around the nucleus, with very few mitochondria migrating to the cell periphery. However in vivo, the influence of this knockout on mitochondrial movement is poorly understood. The Wilcox lab hypothesizes that when the Miro1 protein is knocked out within astrocytes, deregulation of the neurons will lead to hyperactivity and possibly seizures within mice. Through post-natal electroporation and a tamoxifen-induced knockout model, we have generated mice that lack Miro1 in astrocytes. The impact of this knockout on astrocyte morphology and function was then analyzed via immunohistochemistry and the whole-cell patch clamp technique. This analysis provides insight into the role of Miro1 in astrocyte functioning. |
