Disrupted Synaptic Remodeling Due to a Loss of Interleukin-33 Signaling
Interactions between neurons and glia are required for healthy synaptic remodeling, the formation and removal of synapses, and in developing a mature neural circuit. Neurodevelopmental disorders like autism and schizophrenia are devastating outcomes as a result of faulty circuit and synapse formation. Recently published work from the Molofsky lab has shown that developing astrocytes release an innate immune molecule, interleukin-33 (IL-33). This molecule signals to microglia to remove excess synapses from neurons. But it is unclear how circuits and neuronal activity are affected when the receptor for IL-33 (ST2) on microglia is lacking. We hypothesize that microglia lacking ST2 will have abnormal synaptic remodeling. To investigate this further, we will modulate the exposure mice have to light stimulus during the critical period of development for the mouse visual system. The amount of light that a mouse sees during this critical period will result in different rates of synaptic remodeling and neuronal activity. This will allow us to gain insight on the role of immune signaling in brain development.
Message to Sponsor
- Major: Molecular and Cell Biology
- Sponsor: Rose Hills Experience
- Mentor: Ilia Vainchtein