Professor
Office: VBR 211
E-Mail: britter@vetmed.wsu.edu
Phone: (509) 335-8114
"Knowing
When to Stop. Neurobiology of Controlling Food Size", WSU Universe
Magazine, 1997.
"Why Can't we Stop
Eating? Rats Develop Immunity to Fat", WSU Universe Magazine.
"
Gut
Feelings: Decoding the Signals that Control Appetite", WSU The
Innovators Series.
Research Interests
Obesity and diabetes are major causes of illness and death
worldwide.
In the United States, one out of every three people is obese, and
obesity is associated with marked increases in the incidence of
cardiovascular, metabolic and neoplastic disease. My research group
investigates neural and endocrine controls of appetite and body weight.
We are interested in how signals from the gastrointestinal tract and
body fat are used by the brain to control food intake and body weight.
Current areas of focus include the role of communication between the
hindbrain and the hypothalamus for control of food intake by leptin; the
mechanisms by which gastrointestinal hormones and growth factors act on
the nervous system to reduce food intake; the participation of
viscerosensory neurons and neurotransmitters in control of food intake
and body adiposity. Work in my laboratory is funded by grants from the
National Institute for Neurological Diseases and Stroke and the National
Institute for Diabetes, Digestive and Kidney Diseases.
A hormone-secreting cell (green) making close contact with a nerve
fiber (red) in the wall of the small intestine. Chemical communication
between hormones and nerves in the gastrointestinal tract provides
important signals that influence food intake and body weight.
Biographical Information
Robert C. Ritter, Professor, received a B.S. degree in biology from
Valparaiso University in 1967, a V.M.D. in veterinary medicine from the
University of Pennsylvania in 1971 and a Ph.D. in biology from the
University of Pennsylvania in 1974. He joined W.S.U. as an assistant
professor of physiology in 1974.
Selected Reviews and Commentary
Ritter RC. 2004. Increased food intake and CCK receptor
antagonists: beyond abdominal vagal afferents. Am J Physiol Regul Integr
Comp Physiol 286: R991-993
Ritter RC. 2004. Gastrointestinal mechanisms of
satiation for food. Physiol Behav 81: 249-273
Peters JH, Simasko SM,
Ritter RC. 2006. Modulation of
vagal afferent excitation and reduction of food intake by leptin and
cholecystokinin. Physiol Behav 89: 477-485.
Selected Recent Publications
Covasa M and
Ritter RC. 2005. Reduced CCK-induced Fos
expression in the hindbrain, nodose ganglia, and enteric neurons of rats
lacking CCK-1 receptors. Brain Res 1051: 155-163.
Gillespie BR, Burns GA, and
Ritter RC. 2005. NMDA
Channels Control Meal Size via Central Vagal Afferent Terminals. Am J
Physiol Regul Integr Comp Physiol.
Peters JH, McKay BM, Simasko SM, and
Ritter RC. 2005.
Leptin-induced satiation mediated by abdominal vagal afferents. Am J
Physiol Regul Integr Comp Physiol 288: R879-884.
van de Wall EH, Duffy P, and
Ritter RC. 2005. CCK
enhances response to gastric distension by acting on
capsaicin-insensitive vagal afferents. Am J Physiol Regul Integr Comp
Physiol 289: R695-703.
Czaja K,
Ritter RC, Burns GA. 2006.
N-methyl-D-aspartate
receptor subunit phenotypes of vagal afferent neurons in nodose ganglia
of the rat. J Comp Neurol 496(6):877-85.
Peters JH, Simasko SM,
Ritter RC. 2007. Leptin analog
antagonizes leptin effects on food intake and body weight but mimics
leptin-induced vagal afferent activation. Endocrinology 148: 2878-2885.
Guard DB, Swartz TD,
Ritter RC, Burns GA, and Covasa M.
2009. Blockade of hindbrain NMDA receptors containing NR2 subunits
increases sucrose intake. Am J Physiol Regul Integr Comp Physiol 296:
R921-928.
Guard DB, Swartz TD,
Ritter RC, Burns GA, and Covasa M.
2009. NMDA NR2 receptors participate in CCK-induced reduction of food
intake and hindbrain neuronal activation. Brain Res 1266: 37-44.
PubMed Publications (Note: This PubMed Search may produce additional
"R Ritter" authors.)
