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Research in the Littleton lab is aimed at characterizing the mechanisms by which neurons form synaptic connections, how synapses transmit information, and how synapses change during learning and memory. The lab combines molecular biology, protein biochemistry, electrophysiology and neuroimaging approaches with Drosophila genetics to address these questions. Given defects in synaptic connectivity and function contribute to neurodevelopmental diseases like autism, and loss of synapses is a major feature of neurodegenerative diseases like Alzheimer’s and Parkinson’s, work in the lab also provides critical insights into how diverse neurological diseases damage or disrupt synaptic function. The lab uses the fruitfly Drosophila as a model system for these studies. Despite the dramatic differences in complexity between Drosophila and humans, the molecular components of the synapse and the functional mechanisms they govern appear remarkably similar. Drosophila provides key advantages for this work, as neuronal development is very rapid and can be interrogated with genetic and imaging technologies that can’t be employed in humans. The lab has developed several technologies and toolkits that allow visualization of synapse formation and function in living animals. Using these new transgenic tools to visualize single active zone exocytosis, the lab is characterizing how synapses work, how they undergo plasticity, and how they contribute to both evoked and spontaneous fusion. In addition, the lab is defining the molecular machines that regulate both evoked and spontaneous synaptic transmission, as well as synaptic plasticity.