S192 S.19. Understanding the relationships between psychiatric disorders and pain S.19.03 Neurobiology of fear-induced analgesia D.P. Finn 1 ° , M. Roche 2 , G.K. Ford 3 , K. Rea 3 , W.M. Olango 3 , R.K. Butler 3 , B. Harhen 3 , S.M. Geranton 4 , S.P. Hunt 4 . 1 National University of Ireland Galway, Department of Pharmacology & Therapeutics, Galway, Ireland; 2 National University of Ireland Galway, Department of Physiology, Galway, Ireland; 3 National University of Ireland Galway, Department of Pharmacology and Therapeutics, Galway, Ireland; 4 University College London, Department of Cell and Developmental Biology, London, United Kingdom Fear-conditioned analgesia (FCA) is a survival response ex- pressed as a profound suppression of pain during or follow- ing exposure to conditioned aversive stimuli [1]. A substantial body of evidence now implicates the endogenous cannabinoid (endocannabinoid) and GABAergic systems in the regulation of fear and pain responding. Employing a rat model that combines the formalin test of persistent nociception with classical con- textual fear conditioning, we have investigated the role of the endocannabinoid and GABAergic systems in FCA. Our results demonstrate that pharmacological blockade of the CB 1 receptor prevents, whereas pharmacological inhibition of endocannabinoid degradation enhances, expression of FCA in rats. Some evi- dence for endocannabinoid-opioid interactions during FCA has also been generated. Additionally, we have further investigated the brain regions involved in endocannabinoid-mediated FCA. Our data suggest a key role for the endocannabinoid system in the dorsolateral periaqueductal grey and ventral hippocampus in mediating FCA. We have also used in vivo microdialysis and site-specific intracerebral microinjections to demonstrate a role for GABA in the basolateral amygdala and dorsal periaqueductal grey during fear and pain responding and FCA. Our recent work focusing on the molecular correlates of FCA suggests a role for the immediate early genes c-Fos and Zif268 and the plasticity-related serum- and glucocorticoid-inducible kinase 1 (SGK1). Enhanced understanding of the neurobiology of conditioned fear and associ- ated analgesia, may aid the development of novel approaches for the treatment of pain and anxiety-related disorders. Disclosure statement: The research presented in this paper is financially supported by research grants from Science Foundation Ireland, the Irish Health Research Board, the Irish Research Coun- cil for Science, Engineering and Technology and the International Association for the Study of Pain. References [1] Butler, R.K., Finn, D.P., 2009 Stress-induced analgesia. Progress in Neurobiology 88, 184–202. S.19.04 Altered pain processing in posttraumatic stress disorder E. Geuze 1 ° . 1 University Medical Centre Utrecht, Rudolf Magnus Institute of Neuroscience Department of Psychiatry, Utrecht, The Netherlands Individuals who are exposed to a traumatic event are at risk of developing psychiatric disorders such as posttraumatic stress disorder (PTSD). PTSD is an anxiety disorder characterized by re- experiencing of the event, avoidance of stimuli related to the event, and chronic arousal. Clinical studies have reported that pain expe- rience in persons with PTSD is significantly increased compared to controls, and that chronic pain is a commonly reported symptom of patients with PTSD. However, previous empirical research has also reported that patients with PTSD report a decrease in pain intensity ratings after being exposed to traumatic reminders. This has been purported to be related to opioid mediated stress induced analgesia. Activation of the m-opioid receptor system by endoge- nous opioid peptides has indeed been associated with reductions in sensory and affective ratings of pain experience. Recent advances in neuroimaging techniques have led to a rapid increase in the number of publications that examine the complex neurobiological mechanisms of psychiatric disorders such as PTSD. Several brain areas related to pain processing are implicated in PTSD. Neural correlates of pain processing in PTSD have shown increased activation in the left hippocampus and bilateral insula, as well as decreased activation in the bilateral ventrolateral prefrontal cortex and the right amygdala. Stress induced analgesia has been proposed to play a role in the diminished pain sensitivity witnessed in PTSD. Recent results from a new study investigating the role of traumatic stress on pain processing in PTSD will also be presented. S.19.05 Affective and cognitive aspects of pain processing in borderline personality disorder C. Schmahl 1 ° , I. Niedtfeld 1 , I. Klossika 1 . 1 Central Institute of Mental Health, Psychosomatic Medicine, Mannheim, Germany Background: Patients with Borderline Personality Disorder (BPD) often engage in self-injury to terminate emotional stress associated with reduced pain sensitivity. Experimental painful stimulation in BPD leads to a reduced amygdala activity [1]. Therefore we investigated the interaction between emotional stress and painful simulation (study 1) as well as between anticipation of pain and pain processing (study 2) in patients with BPD. Methods: Both studies compared patients with BPD and healthy controls. In study 1, during event-related fMRI we pre- sented IAPS pictures to induce emotional stress for three seconds and painful vs. non-painful thermal stimuli for the following nine second regulation phase. In study 2, thermal pain thresholds as well as fMRI was measured while anticipation of pain was induced by the announcement of intense pain. Results: In study 1, after initial activation we found decreased amygdala and ACC activation during thermal stimulation indepen- dent of painfulness. Anticipation of pain in study 2 increased heat pain thresholds only in patients, but not in controls. Amygdala deactivation in response to pain anticipation was found in both groups, however the effect was larger in the BPD as compared to the HC group. Discussion: Our results from the emotion regulation study sug- gest that pain stimuli in BPD are processed differently depending on the arousal status. The results from the anticipation study confirm earlier findings of amygdala deactivation during pain anticipation and suggest that this effect is more pronounced in patients with BPD. Both meachnisms may be related to disturbed affect regulation and self-injurious behavior in these patients. References [1] Schmahl, C., Bohus, M., Esposito, F., Treede, R.-D., Di Salle, F., Greffrath, W., Ludaescher, P., Jochims, A., Lieb, K., Scheffler, K., Hennig, J., Seifritz, E., 2006. Neural correlates of antinociception in borderline personality disorder. Archives of General Psychiatry 63, 659–667.