College of Veterinary Medicine

Research in IPN

W. Sue Ritter, Ph.D.

  W. Sue Ritter, Ph.D.

Regent's Professor
Office:  VBR 433
Phone: (509) 335-8113

My laboratory is engaged in anatomical, behavioral and physiological experimentation to identify metabolic events that control the onset of feeding behavior and the neural pathways responsible for monitoring these events. In our work, we utilize drugs which stimulate feeding by selectively blocking intracellular utilization of glucose or fatty acids. Although these drugs block metabolism of glucose and fatty acids throughout the body, stimulation of feeding results from their action on specific metabolic receptor cells.

Our work is focused on localization of these metabolic receptor cells and on tracing the neural pathways from these receptors to parts of the brain which organize feeding behavior. Understanding the basic anatomy and physiology of these particular metabolic controls of food intake will contribute importantly to the overall view of how the nervous system integrates feeding behavior, metabolism and body weight and ultimately achieves metabolic homeostasis.

Biographical Information

Sue Ritter, Professor, received an undergraduate degree in psychology from Valparaiso University (1968) and a Ph.D. in physiological psychology from Bryn Mawr College (1973). She joined the W.S.U. faculty in 1974.  She received the Sahlin Faculty Excellence Award for Research in 2009.

I Wondered as I Wandered, by Sue Ritter, third in The Human Side of Science series.

Recent Publications

Taylor K, Lester E, Hudson BD, Ritter S. Hypothalamic and hindbrain NPY, AGRP and NE increase consummatory feeding responses. Physiol Behav 90(5): 744-750, 2007.

Andrew SF, Dinh TT, Ritter S. Localized glucoprivation of hindbrain sites eleicits corticosterone and glucagon secretion. Am J Physiol Regul Integr Comp Physiol 292(5): R1792-$1798, 2007.

Wiater MF, Hudson BD, Virgin Y, Ritter S. Protein appetite in increased after central leptin-induced fat depletion. Am J Physiol Regul Integr Comp Physiol 293(4): R1468-R1473, 2007.

Li A-J, Dinh TT, Ritter S. Hyperphagia and obesity produced by arcuate injection of NPY-saporin do not require upregulation of lateral hypothalamic orexigenic peptide genes. Peptides 29(10): 1732-1739, 2008.

Li A-J, Wang Q, Dinh TT, Ritter S. Simultaneous silencing of NPY and DBH gene expression in hindbrain A1/C1 catecholamine cells suppresses glucoprivic feeding. J Neurosci 29: 280-287, 2009.

Darling R, Ritter S. 2-Deoxy-D-glucose, but not mercaptoacetate, increases food intake in decerebrate rats. Am J Physiol Regul Integr Comp Physiol 297: R382-R386, 2009.

Hudson DB, Emanuel AJ, Wiater MF, Ritter S. The lipoprivic control of feeding is governed by fat metabolism, not by leptin or adipose depletion. Endocrinology 151: 2087-2096, 2010.

Wu X, Wiater MF, Ritter S. NPAS2 deletion impairs responses to restricted feeding but not to metabolic challenges. Physiol Behav 99: 466-471, 2010 (PMCID: PMC2826533).

Emanuel AJ, Ritter S. Hindbrain catecholamine neurons modulate the growth hormone but not the feeding response to ghrelin. Endocrinology 151: 3237-3246, 2010.

PubMed Publications (Note: PubMed Search may produce additional "S Ritter" authors.)
Last Edited: Jul 03, 2013 9:58 AM   

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