Sue Ritter Professor VCAPP Washingon State University Pullman, WA 99164-6520   Phone: 509-335-8113 Email:sjr@vetmed.wsu.edu   Ph.D. 1973, Physiological Psychology Bryn Mawr College, Pennsylvania     RESEARCH INTERESTS: Neural mechanisms and Circuitry Controlling Energy Homeostasis. RESEARCH SUMMARY: My research is focused on the neural mechanisms and circuitry controlling energy homeostasis. Glucose is the obligatory metabolic fuel for the brain. The brain does not store glucose, but is protected from the lethal consequences of glucoprivation by sensitive receptor mechanisms for early detection of glucose deficit. Glucoreceptive mechanisms are coupled to powerful neural, neuroendocrine and behavioral controls for restoration of normoglycemia. Our work focuses primarily on identification of the neural circuitry for essential glucoregulatory controls: increased adrenal medullary secretion, increased corticosterone and glucagon secretion, and increased food intake. In addition, we are studying the well-known effect of chronic central glucose deficit on suppression of estrus cycling. The data indicate that glucoreceptor cells governing all of these responses are located in the hindbrain. In addition, hindbrain catecholamine neurons are essential for elicitation of these responses, providing the coupling between hindbrain glucoreceptive sites and forebrain or spinal effector neurons for each response. Our goal is to localize and phenotypically define the specific hindbrain glucose-sensing cells required for elicitation of these responses. This area of investigation has importance for several aspects of human health, including obesity and diabetes. REPRESENTATIVE PUBLICATIONS: Ritter, S., and T.T. Dinh. 1997. Pattern of hindbrain Fos expression after 2-Deoxy-D-Glucose (2DG) differs from that after immobilization and footshock stress. Appetite. Koegler, F.H., and S. Ritter. 1998. Injection of galanin into the nucleus of the solitary tract (NTS) stimulates feeding in rats with lesions of the paraventricular nucleus of the hypothalamus. Physiol. Behav. 63(4):521-7. 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. Ritter, S., J.B. Ritter, and L. Cromer. 1999. 2-deoxy-D-glucose and mercaptoacetate induce different patterns of macronutrient ingestion. Physiol. Behav. 66(4):709-15. Wiater, MF, and S Ritter: 1999. Leptin does not attenuate the hyperphagia induced by 2-deoxy-D-glucose (2DG). Ann NY Acad Sci 892: 334. Ritter, S, FH Koegler, and M Wiater: 1999. Effects of metabolic blockade on macronutrient selection. In Neural Control of Macronutrient Selection. H-R Berthoud and RJ Seeley (eds). CRC Press: Boca Raton, FL; pp 189-202. Sanders, NM, and S Ritter: 2000. Repeated 2DG-induced glucoprivation attenuates Fos expression and glucoregulatory responses during subsequent glucoprivation. Diabetes. 49(11):1865-74. Ritter S, Dinh TT, Zhang: Y 2000. Localization of hindbrain glucoreceptive sites controlling food intake and blood glucose. Brain Res 856(1-2):37-47. Ritter, S, K Bugarith, and TT Dinh: 2001. Immunotoxic destruction of distinct catecholamine subgroups produces selective impairment of glucoregulatory responses and neuronal activation. J. Comp. Neurol.432: 197-216. Sanders, NM, and S Ritter: 2001. Acute 2DG-induced glucoprivation or dexamethasone abolishes 2DG-induced glucoregulatory responses to subsequent glucoprivation. Diabetes 50: 2831-2836. Fraley, G, TT Dinh and S Ritter. 2002. Immunotoxic catecholamine lesions attenuate 2DG-induced increase of AGRP mRNA. Peptides 6397: 1-8. Fraley, G. and S. Ritter. 2003. Immunolesion of norepinephrine and epinephrine afferents to the medial hypothalamus alters basal expression and 2DG-induced NPY and AGRP mRNA expression in the arcuate nucleus. Endocrinology 144: 175-183. 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):1357-67. Li AJ and Ritter S 2004 Glucoprivation increases expression of neuropeptide Y mRNA in hindbrain neurons that innervate the hypothalamus. Eur J Neurosci 19: 2147-2154