College of Veterinary Medicine

Research in IPN

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


  R-Ritter

Professor
Office: VBR 411
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.  Obesity cannot develop unless one consumes more calories than one expends.  Therefore, understanding the neural control of food intake and energy expenditure is of major importance to public health. My research group investigates neural and endocrine controls of appetite and body weight.  We are especially interested in how signals from the gastrointestinal tract and body fat alter food intake and metabolism by modulating neural signaling in the hindbrain.  In addition, we are very interested in how neurotransmitters and hormones trigger short- and long-lasting neuroplastic changes in the hindbrain, and how such changes produce alterations in feeding behavior that favor weight gain or weight loss.  Our experimental approach to these issues is multidisciplinary and collaborative, combining neuroanatomy, cell and molecular biology, electrophysiology and behavioral testing.

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.

 

 

 

A coronal hemi-section of the rat hindbrain.  The section has been double stained to reveal activation of an enzyme ERK1/2 that triggers both changes in gene transcription over a period of hours and also triggers rapid changes (within minutes) in the function of proteins in nerve terminals.  Green stating indicates activation of ERK1/2 in nerve cell bodies, which gold staining indicates that ERK1/2 also is activated in the terminals and axons of neurons that carry information from the GI tract to the brain  (From Campos et al., 2012).

 

 

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 (2010) Gastrointestinal peptides and the control of food intake. In: Koob G.F., Le Moal M. and Thompson R.F. (eds.) Encyclopedia of Behavioural Neuroscience.  Volume 1, 559-568.  Oxford:  Academic Press

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: 94-99.

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

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.

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.


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.  In Press.  Electronic version first published May 28, 2013.

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.)

Last Edited: Jul 23, 2013 8:36 AM   

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