Professor
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.)
