The gastrointestinal tract contains as many neurons as the spinal cord and
secretes more hormones than any other organ system in the body. Both the
neural and endocrine populations of the GI tract function semi-autonomously
from other organ systems, but profoundly influence the systemic
physiology of animals both in health and disease.
We are interested in neuronal and
endocrine communication between the gastrointestinal tract and the brain. This
communication is important not only for the control of GI functions but also
plays an important role in hunger, satiety and control of body weight. Using a
combination of neuroanatomical, behavioral, biochemical and physiological
approaches we are investigating the role of gastrointestinal hormones and the sensory innervation of the GI
tract in the control of eating and body weight.
Consequently, we are also interested in the sensitivity of the gastrointestinal
innervations to neuropeptides, the neuroanatomy of and pharmacology of
viscerosensory projections in the brain and the interactions between hormones
from fat with gastrointestinal sensory signal. Our ongoing work is focused on the
mechanism of action of specific gut
peptides and the neurotransmitters that are involved in communicating
gastrointestinal signals to the brain. Work in my
laboratory is funded primarily by grants from the National Institutes of
Health.
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.
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