Robert C. Ritter, V.M.D., Ph.D.

Robert C. Ritter, V.M.D., Ph.D.



Office:  Veterinary and Biomedical Research Building (VBR) room 411
Phone: (509) 335-8114

Bob Ritter Head shot Peru

Current Positions

1988-Present Professor of Physiology, IPN, Washington State University, Pullman, WA


My long-standing research interests are in the neural mechanisms that control food intake and body weight.  NIH-funded efforts in my laboratory focus on satiation signals that arise from the gastrointestinal tract and arrive in the CNS via vagal sensory neurons.  Current research specifically pertains to the role of hindbrain neurotransmitter and neuropeptide receptors in modulating and integrating satiation signals and on hindbrain neuroplastic changes that contribute to control of food intake and body weight.  

Biographical Information

Robert C. Ritter, Professor, earned the B.S. in biology at Valparaiso University in 1967, the V.M.D. degree in veterinary medicine from University of Pennsylvania in 1971 and the PhD in Biology/Neuroscience from University of Pennsylvania in 1974.  He joined the WSU faculty in 1974.  Dr. Ritter is a former NIH Jacob Javits Neuroscience Investigator and has been a visiting Professor of Gastroenterology at the London Hospital Medical School, London England and Visiting Professor of Physiology at Flinders University Medical School, Adelaide S. Australia. He was elected to Washington State Academy of Science in 2013 and president elect for the Society for Study of Ingestive Behavior in 2016. 

Current Funding

NIH Role of Glutamate in the Control of Food Intake, PI


  1. Ritter, R.C. (2011) A tale of two endings: Modulation of satiation by NMDA receptors on or near central and peripheral vagal afferent terminals.  Physiol. Behav.  105(1):94-99.
  2. Wright, J., Campos, C., Herzog, T, Covasa, M., Czaja, K. and Ritter. R.C. (2011)  Reduction of food intake by cholecystokinin requires activation of hindbrain NMDA-type glutamate receptors. Am J Physiol Regul Integr Comp Physiol.  301(2):R448-455.
  3. Zhang J and Ritter RC. (2012) Circulating GLP-1 and CCK-8 reduce food intake by capsaicin-insensitive, nonvagal mechanisms. Am J Physiol Regul Integr Comp Physiol 302: R264-273.
  4. Gallaher ZR, Ryu V, Herzog T, Ritter RC, and Czaja K.  (2012) Changes in microglial activation within the hindbrain, nodose ganglia, and the spinal cord following subdiaphragmatic vagotomy. Neurosci Lett 513: 31-36.
  5. Campos CA, Wright JS, Czaja K, and Ritter RC. (2012) CCK-Induced Reduction of Food Intake and Hindbrain MAPK Signaling Are Mediated by NMDA Receptor Activation. Endocrinology 153(6):2633-2646.
  6. Campos, AC, Shiina, H, Silvas, M, Page, S and Ritter RC.  (2013) Vagal afferent NMDA receptors modulate CCK-induced reduction of food intake through synapsin I phosphorylation.  Endocrinology 154(8):2613-2625.
  7. Campos, CA, Shiina, H, and Ritter, RC.  (2014)  Central vagal afferent endings mediate reduction of food intake by melanocortin3/4 receptor agonist.  J. Neurosci. 34(38): 12636-12645.
  8. Zhao, H, Peters, JH, Zhu, M, Ritter RC, and Appleyard SM. (2015) Frequency-dependent facilitation of synaptic throughput via postsynaptic NMDA receptors in the nucleus of the solitary tract.  J. Physiol. 593: 111-125.
  9. Campos, CA and Ritter, RC.  (2015)  NMDA-type glutamate receptors participate in reduction of food Intake following hindbrain melanocortin receptor activation.  Am J Physiol Regul Integr Comp Physiol.  308(1): R1-9.