|Name:||W. Sue Ritter|
|Department:||Integrative Physiology and Neuroscience|
|Credentials:||1973~Ph.D., Bryn Mawr College, Pennsylvania|
PO Box 647620, Pullman, WA 99164-7620
Neural mechanisms and Circuitry Controlling Energy Homeostasis.
My long-standing research interest and commitment is in neural and endocrine mechanisms controlling food intake and energy homeostasis. My ongoing research investigates the mechanisms through which glucose and fatty acids are detected centrally and peripherally, the neural pathways through which they mediate appropriate responses to reduced availability of those substrates, and the nature of the interaction of these substrates at various levels of homeostatic control. The technical approaches I have focused on to address these issues include behavioral studies of food intake, endocrine and metabolic monitoring at the systemic level, surgical approaches for access to and manipulation of brain or visceral areas of interest, molecular neurosurgery with targeted toxins, neuroanatomical track tracing and assessment of circuit functions (recently including viral tools and optogenetic instrumentation), use of transgenic rats and mice, tissue culture and ratiometric calcium imaging and gene silencing.
Li A-J, Wang Q, Davis H, Wang R, Ritter S. Orexin neurons are activated by hindbrain catecholamine neurons during systemic glucoprivation, submitted 2015.
Li A-J, Wang Q, Davis H, Wang R, Ritter S. Orexin, A enhances feeding in male rats by activating hindbrain catecholamine neurons, submitted 2015.
Li A-J, Wiater MF, Wang Q, Dinh RR, Wang R, Simasko SM, Wank S, Ritter S. Mercaptoacetate stimulates feeding and blocks fatty acid-induced GLP-1 secretion by antagonizing GPR40 fatty acid receptors, submitted 2015.
Darling RA, Kinch D, Zhao H, Li A-J, Simasko SM, Ritter S. Mercaptoacetate and fatty acids exert direct and antagonistic effects on nodose neurons via GPR40 fatty acid receptors. Am J Physiol Regul Integr Comp Physiol 307:R35-43, 2014.
Li AJ, Wang Z, Dinh TT, Powers BR, and Ritter S. Stimulation of feeding by three different glucose-sensing mechanisms requires hindbrain catecholamine neurons. Am J Physiol Regul Integr Comp Physiol 306:R257-264, 2014