David Stellwagen, PhD
cytokine • tumor necrosis factor (TNF) • huntington's disease • amyotrophic lateral sclerosis (ALS) • autism • addiction
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; Malenka RC. Synaptic scaling mediated by glial TNFa. Nature, 2006, 440: 1054-9. PMID: 16547515.
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.
Altimimi HF and Stellwagen D. Persistent synaptic scaling independent of AMPA receptor subunit composition. J Neurosci 2013, 33: 11763-7. PMID: 23864664.
Pribiag H and Stellwagen D. Tumor Necrosis Factor-a downregulates inhibitory neurotransmission through protein phosphatase 1-dependent trafficking of GABAA receptors. J Neurosci 2013, 33(40): 15879-93. PMID: 24089494.