J. Troy Littleton, M.D., Ph.D., is the Menicon Professor of Neuroscience in the Departments of Biology and Brain and Cognitive Sciences and The Picower Institute for Learning and Memory at MIT. Dr. Littleton earned his M.D. and Ph.D. degrees in the Medical Scientist Training Program (MSTP) at Baylor College of Medicine. After completing M.D./Ph.D. studies, Dr. Littleton did postdoctoral work at the Univisity of Wisconsin in Madison before moving to MIT in 2000, where he has been charactering how alterations in synapse formation and function contribute to synaptic plasticity and neurological disease. Dr. Littleton has received numerous awards for his research, including a Helen Hay Whitney Fellowship, a Searle Scholar Award, a Sloan Research Fellowship, a Human Frontiers Science Program Fellowship, the Poitras Scholar Award in Neuroscience and a Packard Foundation Fellowship for Science and Engineering. Currently, Dr. Littleton serves as Director of MIT’s Molecular and Cellular Neuroscience Graduate Program.
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.
9.015J Molecular and cellular neuroscience core I
9.09J Cellular and Molecular Neurobiology
Weiss, S., Melom, J.E., Ormerod, K.G., Zhang, Y.V., Littleton, J.T. (2019) Glial Ca2+ signaling links endocytosis to K+ buffering around neuronal somas to regulate excitability. eLife 8:e44186.
Cunningham, K.L., Littleton, J.T. (2019) Neurons regulate synaptic strength through homeostatic scaling of active zones. J. Cell Biology 5:1434-1435.
Akbergenova, Y., Cunningham, K.L., Zhang, Y.V, Weiss, S., Littleton, J.T. (2018) Characterization of developmental and molecular factors underlying release heterogeneity at Drosophila synapses. eLife 7:e38268.
Guan, Z., Bykhovskaia, M., Jorquera, R.A., Sutton, R.B., Akbergenova, Y., Littleton, J.T. (2017) A Synaptotagmin suppressor screen indicates SNARE binding controls the timing and Ca2+ cooperativity of vesicle fusion. eLife 6:e28409.
Akbergenova, Y., Littleton, J.T. (2017) Pathogenic Huntington alters BMP signaling and synaptic growth through local disruptions of endosomal compartments. J. Neuroscience 37:3425-3439.