Professor
E-Mail: sjr@vetmed.wsu.edu
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 W.S.U.s faculty in
1974.
I Wondered as
I Wandered, by Sue Ritter, third in The Human Side of Science
series.
Selected Publications
Ritter, S., N.Y. Calingasan, B. Hutton and T.T. Dinh. 1992. Cooperation
of central and peripheral neural systems in monitoring metabolic events
controlling feeding behavior. In: Neuroanatomy and Physiology of
Abdominal Vagal Afferents, S. Ritter, R.C. Ritter and C.D. Barnes (Eds).
CRC Press, Boca Raton, FL. 249-277.
Ritter, S., and T.T. Dinh. 1994. 2-Mercaptoacetate and 2-deoxy-d-glucose
induce Fos-like immunoreactivity in rat brain. Brain Res. 641: 111-120.
Singer, L.K. and
S. Ritter. 1994. Differential effects of infused
nutrients on 2DG- and MA-induced feeding. Physiol. Behav. 56: 193-196.
Singer, L.K. and
S. Ritter. 1996. Intraventricular glucose blocks
feeding induced by 2-deoxy-D-glucose but not mercaptoacetate. Physiol.
Behav. 59: 921-923.
Ritter, S., L.K. Singer, and A. Scheurink. 1995. 2-Deoxy-d-Glucose but
not mercaptoacetate increases Fos-like immunoreactivity in adrenal
medulla and sympathetic preganglionic neurons. Obesity Res. 3(5):
729S-734S.
Ritter, S., and B. Hutton. 1995. Mercaptoacetate-induced feeding is
impaired by central nucleus of amygdala lesions. Physiol. Behav. 58:
1215-1220.
Koegler, F.H. and
S. Ritter. 1996. Feeding induced by pharmacological
blockade of fatty acid metabolism is selectively attenuated by hindbrain
injections of the galanin receptor antagonist, M40. Obesity Res. 4:
329-336.
Singer, L.K., P. Magluyan, and
S. Ritter. 1996. The effects of low,
medium and high fat diets on 2-deoxy-d-glucose (2DG)- and mercaptoacetate (MA)-induced feeding. Physiol. Behav. 60: 321-323.
Ritter, S., Llewellyn-Smith, I., Dinh, T.T. 1998. Subgroups of hindbrain
catecholamine neurons are selectively activated by 2-deoxy-D-glucose
induced metabolic challenge. Brain Research 805: 41-54
Fraley, G.S., and
S. Ritter. 2003. Immunolesion of norephinephrine and
epinephrine afferents to medial hypothalamus alters basal and
2DG-induced NPY and AGRP mRNA expression in the arcuate nucleus.
Endocrinology 144:75-83.
Ritter, S., A.G. Watts, T.T. Dinh, G. Sanchez-Watts, and C. Pedrow.
2003. Immunotoxin lesion of hypothalamically-projecting norepinephrine
and epinephrine neurons differentially effects circadian and
stressor-stimulated corticosterone secretion. Endocrinology 144 (4):
1357-1367.
I'Anson H., Sundling L.A., Roland S.M.,
Ritter S. 2003. Immunotoxic
destruction of distinct catecholaminergic neuron populations disrupts
the reproductive response to glucoprivation in female rats.
Endocrinology 144: 4325-4331.
PubMed Publications (Note: PubMed Search may produce additional "S
Ritter" authors.)
