(selective serotonin reuptake inhibitors) can be also prescribed in comorbid depression [1]. Structural and functional differences in the anterior cingulate cortex (ACC), which is part of the pain regulatory system, have been observed several times in migraine, but the role of the serotonergic system in this process is poorly understood [2]. In this study we investigated the effect of acute serotonergic challenge on ACC activation in migraine without aura patients. Changes in brain activation following 7.5 mg citalopram, an SSRI, were measured in 27 healthy and 6 migraine volunteers using within-subject, placebo-controlled, double-blind, randomized design with a 30 minutes-long challenge pharmacological fMRI ( phMRI). The two scanning sessions, placebo and citalopram respectively, were separated by at least two weeks. The infusion started after 10 minutes baseline. During the scan subjects rested eyes-opened, viewing a blank screen. The phMRI images were acquired at a 3T MRI scanner (Achieva 3T, Philips Medical System) using a BOLD-sensitive T2*-weighted echo-planar pulse sequence (TR = 2,500 ms, TE = 30 ms, FOV: 240 × 240 mm 2 ) with 3 mm × 3 mm in-plane resolution and 3 mm slice thickness. Imaging data were analysed using Statistical Parametric Mapping (SPM 12, Friston, The Welcome Department of Cognitive Neurology, London, UK) for MATLAB using phMRI analysis method first described by McKie et al. [3]. The ACC region of interest was selected according to Talariach Demon atlas with wfu_pickatlas. The activation changes over time in ACC during and after citalopram infusion were obtained by time x drug interaction F-test. The primary threshold was uncorrected p = 0.001 and the secondary threshold was Family Wise Error corrected peak level p-value of 0.05, with cluster size limit of 5 voxels. We found significant differences in ACC activation between migraine and control subjects: two clusters were observed in the right ACC, one at x = 15, y = 38, z = 8 coordinates (cluster size = 9 voxels, Z = 4.14, p(FWE) = 0.006) and one at x = 9, y = 41, z = −4 (cluster size = 6 voxels, Z = 3.80, p(FWE) = 0.022) in Montreal Neurological Institute (MNI) space. The extracted time-series showed that in the first 8 minutes after infusion the activation of ACC in migraine patients was significantly higher than in controls. While ACC activation increase was found in controls after citalopram infusion in an earlier study [3], our findings clearly demonstrate that migraine patients are more sensitive to citalopram challenge, since they have increased ACC activation compared to the control group especially in the first few minutes of drug response. These results are in line with the hypothesis that migraine is a stress related disorder, as these patients are more sensitive to environmental and sensory factors e.g. lack of sleep, specific food and drinks and psychosocial or even pharmacologic stress [4]. The altered response to citalo- pram in migraine patients may be the result of imbalance between the different neurotransmitter systems that lead to the emergence of migraine. Reference(s) [1] Finocchi, C., Villani, V., Casucci, G., 2010. Therapeutic strategies in migraine patients with mood and anxiety disorders: clinical evidence. Neurol Sci, 31(Suppl 1), S95–98. [2] May, A., 2009. New insights into headache: an update on functional and structural imaging findings. Nat Rev Neurol, 5(4), 199–209. [3] McKie, S., Del-Ben, C., Elliott, R., Williams, S., del Vai, N., Anderson, I., Deakin, J.F., 2005. Neuronal effects of acute citalopram detected by pharmacoMRI. Psychopharmacology (Berl), 180(4), 680–686. [4] Sauro, K.M., Becker, W.J., 2009. The stress and migraine interaction. Headache, 49(9), 1378–1386. Disclosure statement: The study was supported by the Hungarian Academy of Sciences (MTA-SE Neuro- psychopharmacology and Neurochemistry Research Group) and by the Hungarian Academy of Sciences and the Hungarian Brain Research Program – Grant No. KTIA_NAP_13-2-2015-0001 (MTA-SE-NAP B Genetic Brain Imaging Migraine Research Group). The sponsors funded the work, but had no further role in the design of the study, in data collection or analysis, in the decision to publish, or in the preparation, review, or approval of the manuscript. The authors report no conflict of interest. P.2.020 Early modulation of the endocannabinoid tone prevents molecular and behavioral alterations in MAM model of schizophrenia T. Stark 1* , R. Di Marco 2 , J. Ruda-Kucerova 1 , G. Giurdanella 2 , V. Pekarik 3 , Z. Babinska 1 , S. Salomone 2 , R. Mechoulam 4 , F. Drago 2 , A. Sulcova 5 , V. Micale 5 . 1 Masaryk University, Department of Pharmacology, Brno, Czech Republic; 2 University of Catania, Department of Biomedical and Biotechnological Sciences, Catania, Italy; 3 Masaryk University, Department of Physiology, Brno, Czech Republic; 4 Hebrew University of Jerusalem, Insitute for Drug Research, Jerusalem, Israel; 5 CEITEC Masaryk University, Department of Pharmacology, Brno, Czech Republic Recent data suggest that schizophrenia (SCZ) may originate from abnormal central nervous system develop- ment that becomes evident in adulthood [1], while Behavioural and systems S41