sRAGE concentration was elevated in schizophrenia compared to healthy controls. Our data support the hypothesized involvement of glia cells in the pathogenesis of schizophrenia. Not only S100B is enhanced in schizophrenic patients, also the concentration of its soluble decoy receptor is increased, providing further evidence of a dysregulated astrocytic balance between inflammatory and neuro- protective mechanisms in schizophrenia. doi:10.1016/j.bbi.2009.06.108 104. Strain differences in restraint stress induced brain IL-1, IL-6, COX2 V.M. Porterfield, Z.R. Zimomra, J.D. Johnson Kent State University, Biological Sciences, Kent, OH 44242, United States Exposure to stressors such as tailshock and footshock elevate hypothalamic IL-1, while exposure to swim, predator odor, and restraint stress do not. Some propose that the use of shock may cause tissue damage and/or bacterial translocation that initiate cytokine production. Recent studies suggest that induction of brain IL-1 may depend more on levels of brain norepinephrine than stressor severity. The aim of the current study was to compare brain cytokine responses to acute restraint stress in Sprague–Daw- ley and Fischer344 (a more stress responsive strain) rats. Animals were exposed to restraint stress or stayed in their home cage to serve as controls and sacrificed after 1 h for analysis of IL-1, IL-6 and COX2 mRNA or after 2 h for analysis of IL-1 protein. Exposure to restraint did not significantly increase hypothalamic cytokines in Sprague–Dawley rats, but did significantly elevate hypothalamic IL-1 mRNA and IL-1 protein in Fischer344 rats (IL-6 and COX2 were not altered). Choroid plexus was also analyzed and restraint stress elevated IL-6 mRNA, but not IL-1 or COX2 mRNA, suggesting that choroid plexus may contribute to brain IL-6, but not hypotha- lamic IL-1 levels. These data support our hypothesis that a critical threshold of brain norepinephrine is necessary to stimulate brain cytokines and that tissue damage and/or bacterial translocation are likely not the mechanism by which stressors induce brain cytokines. Supported by MH77004. doi:10.1016/j.bbi.2009.06.109 105. Meditation, consternation and inflammation: The effect of compassion focused mind training on physiological and behav- ioral responses to psychosocial stress C. Raison Emory University School of Medicine, Psychiatry and Behavioral Sciences, 298 Sutherland Place NE, Atlanta, GA 30307, United States Meditation has gained increasing currency as an intervention for a wide range of stress-related emotional and medical conditions. However, less is known regarding mechanisms by which meditation may benefit health. This talk addresses this issue by presenting recent data on the effect of a Tibetan–Buddhist-based compassion meditation technique on physiological and behavioral responses to psychosocial stress. More specifically, we will present data from two study cohorts suggesting that the practice of compassion med- itation is associated with reductions in autonomic and innate immune responses to the Trier Social Stress Test (TSST), a widely- used, standardized laboratory-based psychosocial stress paradigm. The talk will conclude with a discussion of the potential relevance of specific meditation procedures for affecting health-relevant stress pathways. doi:10.1016/j.bbi.2009.06.110 106. Acute psychosocial stress induces short-term catecholamine resistance of TNF-alpha, but not of IL-6 production in healthy young men N. Rohleder a , J.M. Wolf a , C. Kirschbaum b a Brandeis University, Psychology, 415 South Street, Waltham, MA 02454, United States b Technische Universität Dresden, United States We have previously shown that psychosocial stress induces acute changes in glucocorticoid (GC) sensitivity of pro-inflammatory cyto- kine production. Inflammatory responses, however, are also regu- lated by hormones of the SAM axis. The current study, therefore, aimed at investigating the effects of acute stress exposure on the cat- echolamine sensitivity of immune cells. Twenty-one healthy male participants were subjected to the Trier Social Stress Test (TSST) on two consecutive days. Blood samples were taken before and repeatedly after stress and whole blood was stimulated with lipo- polysaccharide and incubated with increasing concentrations of epi- nephrine (E) and norepinephrine (NE) for 18 h. Tumor-necrosis- factor (TNF) alpha and interleukin (IL)-6 were then measured in cul- ture supernatants. Overall, incubation with E and NE induced dose- dependent suppression of TNF-alpha (F = 77.66; p < 0.001), and IL-6 production (F = 28.79; p < 0.001), with significantly stronger sup- pression of TNF-alpha (F = 26.36; p < 0.001). Acute stress, however, induced relative resistance of TNF-alpha (F = 11.38; p < 0.001), but not IL-6 (F = 1.56; p = 0.22) to the inhibitory signals of E and NE. The present findings show that changes in inflammatory target tis- sues sensitivity in response to acute psychosocial stress are not re- stricted to glucocorticoids, but that the catecholamine sensitivity of inflammatory cells is stress-responsive as well. Most importantly, catecholamine sensitivity of immune cells appears to display a high- er cytokine specificity compared to GC sensitivity. doi:10.1016/j.bbi.2009.06.111 107. A systemic LPS challenge does not alter central Beta2-adre- noceptor expression or reponsiveness K.M. Ryan a , A. Harkin b , T.J. Connor a a Neuroimmunology Research Group, School of Medicine & Trinity College Institute of Neuroscience, Lloyd Building, Trinity College, Dublin 2, Ireland b Neuropsychopharmacology Research Group, School of Pharmacy & Pharmaceutical Sciences & Trinity College Institute of Neuroscience, Trinity College, Dublin 2, Ireland The endogenous anti-inflammatory and neurotrophic actions of noradrenaline in the central nervous system are mediated by microglial and astrocytic beta2-adrenoceptors. We have previously shown that in vitro exposure of primary mixed glial cells to an inflammatory challenge with LPS + IFN-gamma down-regulates beta2-adrenoceptor mRNA and cell surface expression, and reduces receptor responsiveness as indicated by blunted cAMP accumulation in response to the agonist salbutamol, effects that could inhibit the beneficial effects of endogenous noradrenaline. In the current study we examine the impact of a systemic inflammatory challenge on S54 Abstracts / Brain, Behavior, and Immunity 23 (2009) S25–S64