Ph.D., Princeton University, 1982
Faculty » B. Glenn Stanley
Our research is focused on defining the brain mechanisms that control eating behavior. We hope to learn how the normal and abnormal function of these mechanisms contribute to natural eating behavior, as well as to disturbances of eating behavior and body weight control. Equally important, we hope to reveal principles of neural integration that are relevant to a broad range of brain functions. The type of questions we ask are: which physiological and environmental factors are responsible for activating eating-control neurocircuits; what are the specific neural pathways and neurotransmitters which comprise these circuits and; what are the behavioral/physiological consequences of their activation? We are using three complementary approaches to address these issues in animals as described below.
Central Microinjection. Minute quantities of certain neurotransmitters, when injected directly into specific brain areas, can cause animals to perform complex behaviors similar to those that occur naturally. For example, we have shown that microinjections of neuropeptide Y into specific areas of the hypothalamus can cause animals to eat and, with chronic stimulation, to develop massive obesity. By determining which neurotransmitters act similarly and the brain areas where they are effective, we can begin to reveal the specific neurochemicals and brain sites involved in controlling eating behavior and body weight gain.
Measurement of Neurotransmitter Release. Here, instead of modulating brain chemistry and then measuring the corresponding changes in behavior, we manipulate the animal's behavior and then use biochemical techniques to measure the corresponding changes in brain chemistry. For example, we have shown that norepinephrine, another neurotransmitter that causes eating when injected into a certain brain area, is also normally released from this same brain area during natural eating behavior.
Imaging Brain Activity. More active brain areas have higher metabolic rates. Therefore, we can use metabolic imaging techniques to derive a picture of the specific brain areas activated during eating behavior. Using this approach, we are identifying the neuronal sites and brain pathways which are activated by central neurotransmitter injections that produce eating, as well as those naturally activated during this behavior.
Hettes, S.R., Gonzaga, J.W., Heyming, T.W., Nguyen, J.K., Perez, S., Stanley, B.G. (2010) Stimulation of lateral hypothalamic AMPA receptors may induce feeding in rats. Brain Research, 1346, 112-120.
Turenius, C.I, Htut, M.H., Prodon, D.A., Ebersole, P.L., Ngo, P.T., Lara, R.N., Wilczynski, J.L. and Stanley, B.G. (2009) GABAA receptors in the lateral hypothalamus as mediators of satiety and body weight regulation. Brain Research, 1262, 16-24.
Turenius, C.I., Charles, J.R., Tsai, D.H., Ebersole, P.L., Htut, M.H., Ngo, P.T. and Stanley, B.G. (2009) The tuberal lateral hypothalamus is a major target for GABAA but not GABAB-mediated control of food intake. Brain Research, 1283, 65-72.
Khan, A.M., Ponzio, T.A., Sanchez-Watts, G., Stanley, B.G., Hatton, G.I., and Watts, A.G. (2007) Catecholaminergic control of mitogen-activated protein kinase signaling in paraventricular neuroendocrine neurons in vivo and in vitro: a proposed role during glycemic challenges. Journal of Neuroscience, 27(27), 7344-7360.
Hettes, S.R., Heyming, T.W., and Stanley, B.G. (2007) Stimulation of lateral hypothalamic kainate receptors selectively elicits feeding behavior. Brain Research, 1184, 178-185.
Lee, S.W. & Stanley, B.G. (2005) NMDA receptors mediate feeding elicited by neuropeptide Y in the lateral and perifornical hypothalamus. Brain Research, 1063, 1-8.
Duva, M.A., Tomkins, E.M., Moranda, L.M., Kaplan, R., Sukhaseum, A., Stanley, B.G. (2005) Origins of lateral hypothalamic afferents associated with N-methyl-D-aspartic acid-elicited eating studied using reverse microdialysis of NMDA and Flurogold. Neuroscience Research, 52(1), 95-106.
Duva, M.A., Siu, A., and Stanley, B.G. (2005) Antagonist of NMDA receptors alters lipoprivic eating elicited by 2-mercaptoacetate. Physiology and Behavior, 83, 787-791.
Khan, A.M., Cheung, H.H., Gillard, E.R., Palarca, J.A., Welsbie, D.S., Gurd, J.W., and Stanley, B.G. (2004) Lateral hypothalamic signaling mechanisms underlying feeding stimulation: Differential contributions of Src family tyrosine kinases to feeding triggered either by NMDA injection or by food deprivation. Journal of Neuroscience, 24(47), 10603-10615.
Hettes, S.R., Gonzaga, J. Heyming, T.W., Perez, S., Wolfsohn, S. & Stanley, B.G. (2003) Dual roles in feeding for AMPA/kainate receptors: receptor activation or inactivation within distinct hypothalamic regions elicits feeding behavior, Brain Research, 992, 167-178.
Duva, M.A., Tomkins, E.M., Moranda, L.M., Kaplan, R., Sukhaseum, A., Bernardo, J.P. & Stanley, B.G. (2002) Regional differences in feeding and other behaviors elicited by N-methyl-D-aspartic acid in the rodent hypothalamus: a reverse microdialysis mapping study, Brain Research, 925, 141-147.
Blevins, J.E. Stanley, B.G. & Reidelberger, R.D. (2002) DMSO as a vehicle for central injections: Tests with feeding elicited by norepinephrine injected into the paraventricular nucleus, Pharmacology Biochemistry and Behavior, 71(1-2), 277-282.
Duva, M.A., Tomkins, E.M., Moranda, M., Kaplan, R. Sukhaseum, A., Jimenez, A. & Stanley, B.G. (2001) Reverse microdialysis of N-methyl-D-aspartic acid into the lateral hypothalamus of rats: effects on feeding and other behaviors, Brain Research, 921, 122-132.