Office: VBR 415
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.
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
I Wondered as
, by Sue Ritter, third in The Human Side of Science
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.
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