Glial cells are non-neuronal cells in the central nervous system (CNS) that carry out many "support" functions. Among the glia, astrocytes operate as central coordinators of many functions such as synaptic transmission, brain development, and the damage response. My research focuses on astrocytes during the damage response, specifically in the context of demyelinating disorders such as Multiple Sclerosis (MS). Astrocytes respond to CNS damage by becoming "reactive", a state in which they take on a range of new forms and functions. During and immediately following injury, reactive astrocytes are key in limiting the spread of damage as well as facilitating cleanup and repair processes. However, the prolonged reactivity of astrocytes can be harmful since they produce neuroinflammation which can contribute to damage and prevent repair.

My research makes use of the designer G-protein coupled receptors (DREADDs), hM3Dq and hM4Di, to selectively enhance or suppress astrocyte reactivity in mouse models of demyelinating disease. This work investigates how modulation of reactivity within different phases of disease affects both neurobiological and behavioral consequences of demyelination. Ultimately, the aim of this work is to identify important pathways that control astrocyte reactivity in response to demyelinating injury, in order to find new potential treatment approaches for demyelinating disorders.