Julie A. Coffield is an Associate Professor of Toxicology/Neuroscience in the College of Veterinary Medicine's Department of Physiology and Pharmacology. Dr. Coffield is a graduate of the University of Wisconsin-Madison where she received both her D.V.M. and Ph.D. degrees. She is the course coordinator and principal instructor for Principles in Veterinary Toxicology, Principles of Small Animal Toxicology and Principles of Large Animal Toxicology, and participates in several graduate courses including Mammalian Cell Physiology, and Neurophysiology. Dr. Coffield is also the Graduate Coordinator for the Interdisciplinary Program in Toxicology and a member of the Biomedical Health Sciences Institute. Dr. Coffield's research interests focus on neurotoxic agents that alter synaptic transmission. In particular, she studies the actions of toxins such as the Clostridial neurotoxins (Botulinum and Tetanus) at the mammalian neuromuscular junction. She is a member of the Society for Neuroscience, the Southeastern Society of Toxicology, and the Community of Science, and is a past president of the UGA Neuroscience Chapter.

The major objective of Dr. Coffield's NIH-funded research program is the identification and characterization of the neural membrane receptors and intracellular protein targets of Botulinum toxin at the mammalian neuromuscular junction. Botulinum toxin, the most poisonous substance known, is the agent responsible for the fatal disease botulism. Botulinum toxin is one of the CDC's six Category A biological agents of greatest concern for use as a biological weapon. This agent is extremely potent, easy to produce and transport, and has high potential for morbidity and mortality, making it a major threat as a bioweapon. The principal target site for Botulinum toxin action is the neuromuscular junction, where minute amounts of the toxin cause paralysis and eventual death by inhibiting the release of acetylcholine. Currently, there are no effective treatment measures for botulism, and death usually results from paralysis of the respiratory muscles. Although both an antitoxin and a vaccine are available, antitoxin is not very effective once symptoms appear, and general use of the vaccine is unlikely in light of the expanding use of botulinum toxin by the medical community to treat a variety of neuromuscular disorders.

At work in the Coffield lab

More recently, Dr. Coffield's research group has isolated and studied membrane proteins of the neuromuscular junction that bind botulinum toxins serotypes important in human poisonings (serotypes A, B). These binding proteins are potential candidates for membrane receptors that mediate the very selective targeting and uptake of the toxin into the nerve terminal of the neuromuscular junction. Identification and characterization of these membrane receptors will be crucial to the development of effective countermeasures to Botulinum toxin exposure.