null David Stellwagen, PhD
neuro-immune interactions • inflammation • tumor necrosis factor (TNF) • synaptic plasticity • glia • stress • addiction • autism • amyotrophic lateral sclerosis (ALS) • Huntington's Disease
My research focuses on how inflammation regulates the function of neurons, particularly the synaptic connections between neurons. We have discovered that inflammatory signals are used to maintain normal levels of neuronal activity (homeostasis), and this is achieved through the regulation of synaptic strength. We are investigating how this contributes to the change in brain function observed during many disorders, as most neurological diseases are accompanied by inflammation. In particular, we are investigating the compensatory mechanisms that may be engaged during neurodegenerative disease and psychiatric disorders such as addiction and autism.
Stellwagen D, Kemp GM, Valade S, Chambon J. Glial regulation of synaptic function in models of addiction. Curr Opin Neurobiol 2019, 57: 179-85. PMID: 31163290.
Lewitus G, Konefal SC, Greenhalgh AD, Pribiag H, Augereau K, Stellwagen D. Microglial TNF suppresses cocaine-induced synaptic plasticity and behavioral sensitization. Neuron 2016, 90(3): 483-91. PMID: 27112496.
Pribiag H, Peng H, Shah W, Stellwagen D, Carbonetto S. Dystroglycan mediates homeostatic synaptic plasticity at GABAergic synapses. PNAS 2014, 111(18): 6810-5. PMID: 24753587.
Lewitus G, Pribiag H, Duseja R, St-Hilaire M, Stellwagen D. An adaptive role of TNFα in the regulation of corticostriatal synapses. J Neurosci 2014, 34(18): 6286-6293. PMID: 24790185.
Stellwagen D; Malenka RC. Synaptic scaling mediated by glial TNFa. Nature, 2006, 440: 1054-9. PMID: 16547515.