Robert C. Ritter
Room: VBR 411
Current Positions1988-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 InformationRobert 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 FundingNIH Role of Glutamate in the Control of Food Intake, PI
- Zhao H, Peters JH, Zhu M, Ritter RC, and Appleyard SM (2014) Frequency-dependent facilitation of synaptic throughput via postsynaptic NMDA receptors in the nucleus of the solitary tract J Physiol 593(1):111-125 PMID: 25281729 PMCID: PMC4293058
- Ritter RC (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), 94-9 PMID: 21382391 PMCID: PMC3181280
- Wright J, Campos C, Herzog T, Covasa M, Czaja K, Ritter RC (2011) Reduction of food intake by cholecystokinin requires activation of hindbrain NMDA-type glutamate receptors Am J Physiol Regul Integr Comp Physiol 301(2), R448-55 PMID: 21562094 PMCID: PMC3154714
- Zhang J, 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(2), R264-73 PMID: 22031786 PMCID: PMC3349390
- Gallaher ZR, Ryu V, Herzog T, Ritter RC, Czaja K (2012) Changes in microglial activation within the hindbrain, nodose ganglia, and the spinal cord following subdiaphragmatic vagotomy Neurosci Lett 513(1), 31-6 PMID: 22342909 PMCID: PMC3302977
- Campos CA, Wright JS, Czaja K, Ritter RC (2012) CCK-Induced Reduction of Food Intake and Hindbrain MAPK Signaling Are Mediated by NMDA Receptor Activation Endocrinology 153(6), 2633-46 PMID: 22508518 PMCID: PMC3359610
- Campos CA, Shiina H, Silvas M, Page S, Ritter RC (2013) Vagal afferent NMDA receptors modulate CCK-induced reduction of food intake through synapsin I phosphorylation Endocrinology 154(8), 2613-25 PMID: 23715865 PMCID: PMC3713210
- Campos CA, Shiina H, Ritter RC (2014) Central vagal afferent endings mediate reduction of food intake by melanocortin3/4 receptor agonist J Neurosci 34(38), 12636-45 PMID: 25232103 PMCID: PMC4166153
- Campos CA, 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 PMID: 25394828 PMCID: PMC4281681