Alan S Lewis
animal models;aggression;nicotine;nicotinic acetylcholine receptors;ion channels;neurodevelopmental disorders; autism spectrum disorder; schizophrenia
Aggression is comorbid with numerous neuropsychiatric disorders across the lifespan. Understanding is limited as to how such conditions might increase predisposition to aggression. Furthermore, treatment for aggression, which includes both behavioral and pharmacological approaches, can be incompletely effective, and in the case of pharmacotherapy, places patients at high risk for serious side effects. The overall goal of my current research is to identify how the nicotinic acetylcholinergic receptor system governs aggressive behavior in preclinical models, with the ultimate goal of translating these findings into improved treatments for clinical populations.
- Lewis AS, Picciotto MR (2013) High-affinity nicotinic acetylcholine receptor expression and trafficking abnormalities in psychiatric illness. Psychopharmacology (Berl) 229:477-485.
- Lewis AS, Schwartz E, Chan CS, Noam Y, Shin M, Wadman WJ, Surmeier DJ, Baram TZ, Macdonald RL, Chetkovich DM (2009) Alternatively spliced isoforms of TRIP8b differentially control h channel trafficking and function. Journal of Neuroscience 29:6250-6265.
- Lewis AS, Vaidya SP, Blais CA, Liu Z, Stoub TR, Brager DH, Chen X, Bender RA, Estep CM, Popov AB, Kang CE, van Veldhoven PP, Bayliss DA, Nicholson DA, Powell CM, Johnston D, Chetkovich DM (2011) Deletion of the HCN channel auxiliary subunit TRIP8b impairs hippocampal Ih localization and function and promotes antidepressant behavior in mice. Journal of Neuroscience 31:7424-7440.
- Han Y, Noam Y, Lewis AS, Gallagher JJ, Wadman WJ, Baram TZ, Chetkovich DM (2011) Trafficking and gating of hyperpolarization-activated cyclic nucleotide-gated channels are regulated by interaction with tetratricopeptide repeat-containing Rab8b-interacting protein (TRIP8b) and cyclic AMP at distinct sites. Journal of Biological Chemistry 286:20823-20834.
- Lewis AS, Chetkovich DM (2011) HCN channels in behavior and neurological disease: too hyper, or not active enough? Molecular and Cellular Neuroscience 46:357-67.