William Atchison, Ph.D.
- A-C, Environmental Faculty, Neuropharmacology Faculty
Professor, Pharmacology & Toxicology
Dr. William Atchison
B331A Life Sciences
1355 Bogue Street
East Lansing, MI 48824
Fields of Interest: Research in my lab is directed at understanding the basis of cellular neurotoxicity, especially at synapses.
- 1974 - B.S., Molecular Biology, University of Wisconsin
- 1978 - M.S., Pharmacology, University of Wisconsin
- 1980 - Ph.D., Pharmacology, University of Wisconsin
- 1981-82 - Postdoctoral Fellow, Northwestern University
- 1982-87 - Assistant Professor, Pharmacology & Toxicology, Michigan State University
- 1987-91 - Associate Professor, Pharmacology & Toxicology, Michigan State University
- 1991-present - Professor, Pharmacology & Toxicology, Michigan State University
The nervous system has its limited capacity to repair tissue damage and minimal neurogenesis. Coupled with the high energy demands (glucose, O2) of neurons, this makes the neurons system especially susceptible to damage. Research in my lab is directed at understanding the basis of cellular neurotoxicity especially at synapses. These are points at which neurons communicate with effector cells. This toxicity can result from disease process of chemical mediated damages.
A characteristic of many neurological disorders is the remarkably cell specific nature of toxicity. This is clearly evident in neurodegenerative disease such as Parkinson’s Disease and amyotrophic lateral sclerosis (which preferentially target dopaminergic neurons in nigrostriatal pathway, and motor neurons, respectively). A similar phenomenon occurs with chemically-induced neurotoxicity. Understanding the basis for this selective vulnerability- basically a “why me” phenome-non- is a major goal of our research.
Much of our research focuses on understanding cell-selective neurotoxicity of the environmental contaminant methylmercury (MeHg). This metal has been causative of two major outbreaks of neurotoxicity and death- both resulting from consumption of contaminated food. It remains a contemporary concern, especially for pregnant and nursing women, due to the pronounced perinatal toxicity of MeHg.
Differential cellular toxicity is a hallmark of MeHg poisoning, and occurs prominently in the visual system and cerebellum. We are studying cellular targets of MeHg on cerebellar granule cells, which are particularly sensitive to MeHg to identify unique targets that could underlie the cell-specific neurotoxicity. Chief among these are membrane ion channels, both those activated by changes in electrical potential (voltage-gated), as well as those activated by chemical ligands. These include several neurotransmitter receptors, but especially GABAA receptors and voltage-gated Ca2+ channels. These mediate fast synaptic inhibition, and in granule cells control the rate of firing these cells. Block of their function by MeHg could lead to overstimulation of our excitatory transmitter glutamate. This can lead to a form of Ca2+-induced neuronal death known as excitotoxicity.
Another focus in the lab is the study of human neuromuscular diseases. Projects are underway to examine the pathogenesis of a human autoimmune neuromuscular disorder - Lambert Eaton Myasthenic Syndrome, and Amyotrophic Lateral Sclerosis (ALS). In each case studies utilize mouse models of the disease with examination of the pathogenic targets, and disease progression.
Finally, we are involved in projects which interact with colleagues in the Veterinary School. Both deal with known veterinary neurological disorders. Studies are directed at understanding the targets for disease process.
A variety of techniques including electrophysiological recordings of ion channel activity (patch-voltage clamp) and synaptic transmission (intracellular and extracellular microelectrode recording techniques), neurochemical analysis of synaptic function and fluorescent microscopy and digital imaging of intracellular ion concentrations using fluorescent probes such as fura-2. We are also using heterologous expression of recombinant proteins such as GABAA receptors and employ genetic models in mice, and the nematode C. elegans.
- Society of Toxicology- Astra-Zeneca Traveling Lectureship, 2003
- Society of Toxicology Board of Publications Award, “Best paper in Societal Journal”, 1995;
- Michigan State University- All University Excellence in Diversity Award for Sustained Efforts in Excellence in Diversity, 2010
- Michigan State University- Distinguished Faculty Award, 2010
- Supported continuously by the NIH for research since 1980
- NIH Study Section Reviewer and/or Chair since 1989
- Acting Associate Dean for Research, College of Veterinary Medicine, 2010-present
- Neurotoxicology, 1986-present; Associate Editor, 1989-present
- Journal of Pharmacology and Experimental Therapeutics, 1988-2001
- Toxicology and Applied Pharmacology, 1989-2000; Associate Editor, 1990-1995
National & International Society Committees
- Myasthenia Gravis Association, Medical Advisory Board, 1990-1991 (Member); 1991-present (Chair)
- Society of Toxicology, Neurotoxicology Specialty Section, Secretary/Treasurer, 1998-1999; Vice-President, 1999-2000; President, 2000-2001; Past President, 2001-2002
- National Institutes of Environmental Health (NIEHS) Environmental Health Sciences—(1) Review Panel, Chair
- Faculty Advisor, MSU Student Chapter of Okinawan Sanchin-ryu Karate Organization, 2006-present
- Director, Bridges to Ph.D. in Neuroscience Program at Michigan State University, NINDS-sponsored diversity education partnership with University of Puerto Rico in Cayéy
Full List of Publications at MSU Scholars
Omega-conotoxins as experimental tools and therapeutics in pain management. Hannon HE, Atchison WD. Mar Drugs. 2013 Mar 7;11(3):680-99. doi: 10.3390/md11030680. Review. PMID: 23470283
- The role of de novo catecholamine synthesis in mediating methylmercury-induced vesicular dopamine release from rat pheochromocytoma (PC12) cells. Tiernan CT, Edwin EA, Goudreau JL, Atchison WD, Lookingland KJ. Toxicol Sci. 2013 May;133(1):125-32. doi: 10.1093/toxsci/kft025. Epub 2013 Feb 19. PMID: 23425605
- Ca2+ entry pathways in mouse spinal motor neurons in culture following in vitro exposure to methylmercury. Ramanathan G, Atchison WD. Neurotoxicology. 2011 Dec;32(6):742-50. doi: 10.1016/j.neuro.2011.07.007. Epub 2011 Aug 2. PMID: 21839771
- Channelopathies: summary of the hot topic keynotes session. Magby JP, Neal AP, Atchison WD, Pessah IP, Shafer TJ. Neurotoxicology. 2011 Oct;32(5):661-5. doi: 10.1016/j.neuro.2011.06.002. Epub 2011 Jul 2. Review. PMID: 21756936