P.1.i. Basic and clinical neuroscience − Brain imaging and neuro-modulation S301 scale of 1 to 10) but was pulsating with mild photophobia. After the scan she developed a typical migraine attack and described her headache as bilateral, throbbing and 7/10 associated with photophobia. Functional MRI data acquisition was performed at a 3T MRI scanner (Achieva 3T, Philips Medical System) using a T2*-weighted echo-planar imaging sequence (TR = 2.500 ms, TE = 30 ms, slice thickness 3 mm, in-plane resolution 3×3 mm, FOV = 240×240 mm 2 ). To determine changes in the functional connectivity of the DMN a period of 4 minutes from both scans was selected, while the participant was in rest without anything to do and with eyes opened. Imaging data were analysed using Statistical Parametrical Mapping 12 (SPM12) and the CONN toolbox for MATLAB, using seed-to-voxel whole brain temporal correlation analysis, with false discovery rate (FDR) correction at p0.05 significance level with a minimum cluster size limit of 50 voxels on each occasions. During migraine attack all the DMN seeds (e.g., the posterior cingulate cortex, the medial pre- frontal cortex, and left and right lateral parietal cortices) showed decreased connectivity with right inferior temporal cortex, right superior parietal cortex and precuneus bilaterally, and increased connectivity with left postcentral gyrus, pons, thalamus, caudate, posterior insula, frontal and occipital cortices bilaterally. Thus, our findings showed that during spontaneous migraine attack the intrinsic connectivity within the DMN decreased but the functional connectivity between DMN and other networks and the insula increased. Interestingly, during the pharmacologically induced migraine different connectivity pattern emerged showing increased connectivity with several brain areas, but not with regions of the pain matrix [3]. Although our results are based on a single case, these differences in DMN resting state functional connectivity al- terations suggest that spontaneous and pharmacologically induced migraine attacks may evolve through pathological transformations in different brain networks. Thus, our findings emphasise the importance of investigating resting state connectivity changes during spontaneous acute migraine attacks. References [1] Colombo, B., Rocca, M.A., Messina, R., Guerrieri, S., and Filippi, M., 2015. Resting-state fMRI functional connectivity: a new perspective to evaluate pain modulation in migraine? Neurol Sci. 36 Suppl 1, 41−55. [2] Maleki, N. and Gollub, R.L., 2016. What Have We Learned From Brain Functional Connectivity Studies in Migraine Headache? Headache 56, 453–461. [3] Amin, F.M., Hougaard, A., Magon, S., Asghar, M.S., Ahmad, N.N., Rostrup, E., Sprenger, T., and Ashina, M., 2016. Change in brain network connectivity during PACAP38-induced migraine attacks: A resting-state functional MRI study. Neurology 86(2), 180–187. Disclosure statement: The study was supported by the Hungarian Academy of Sciences (MTA-SE Neuropsychopharmacology 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.1.i.006 Myo-inositol prevents ultrastructural alterations provoked by kainic acid-induced status epilepticus in the structure of rat hippocampus M. Zhvania 1° , N. Japaridze 2 , N. Kotaria 3 , T. Bolkvadze 4 , R. Solomonia 5 , G. Lobzhanidze 6 1 Ilia State University, Tbilisi, Georgia; 2 I. Beritashvili Center of Experimental Biomedicine, Brain Ultrastructure and Nanoarchitecture, Tbilsi, Georgia; 3 I. Beritashvili Center of Experimental Bioedicine, Brain Ultrastructure and Nanoarchitecture, Tbilisi, Georgia; 4 I. Beritashvili Center of Experimental Biomedicine, Brain Ultrastructure and Nanoarchitecture, Tbilisi, Georgia; 5 Ilia State University, Institute of Chemical Biology, Tbilisi, Georgia; 6 Ilia tate University, Institute of Chemical Biology, Tbilisi, Georgia Myo-inositol is physiologically important osmolyte and precursor for lipid synthesis. Several data indicate that Myo-inositol could be involved in epilepsy-related activities [1] and [2]. Thus, it was demonstrated that pretreatment with Myo-inositol attenuates the seizure activities and several biochemical alterations provoked by experimentally induced status epilepticus [3] and [4]. Here we in- vestigated if pretreatment with Myo-inositol has positive effect on ultrastructural alterations, initiated by kainic acid-induced status epilepticus. Male adult Wistar rats were used. The animals were treated with: (Group I) − saline; (Group II) − saline and after 30 min interval, with kainic acid at the dose 10 mg/kg; (Group III) − Myo-inositol, at the dose 30 mg.kg, and after 30 min interval, with kainic acid at the dose 10 mg/kg (ten animals in each group). From groups II and III, only animals that developed status epilepticus were selected. The brains were evaluated under electron micro- scope: 2, 14 and 30 days after treatment and the ultrastructure of neurons, synapses, glial cells, extracellular matrix and porosomal complex in the CA1 and CA3 areas of the hippocampus was described. Besides, quantitative analysis of different forms of synapses and morphometric study of main structural parameters of porosomal complex − diameter and depth − were performed. As a result of status epilepticus alterations were observed in both areas of the hippocampus. The most numerous changes were seen in the CA1 area, 14 and 30 days after treatment. Among cells, the most altered were pyramidal neurons. Thus, in these cells peripheral or, in a few cases, total chromatolysis, destruction of mitochondria, vacuolization of different organelles or cytoplasm, the shrinkage of nuclei (the sign of apoptosis) and swelling of dendritic shafts were observed. In some synapses agglutination of synaptic vesicles, the occurrence of huge mitochondria, the swelling of presynaptic terminals, presynaptic terminals with sin- gle but huge vesicles, concentrations of synaptic vesicles close proximity from active zone, and/or osmiophilic inclusions in presynaptic and postsynaptic regions were detected. In some places the extracellular space was abnormally enlarged. Dark, irregular profiles − the rests of degenerative presynaptic terminals or cells, partly engulfed with proliferating astrocytes − were also observed. Some of such alterations were irreversible. Quantitative analysis revealed significant decrease of the number of axo- somtic synapses but no changes in main structural parameters of porosomal complex. The majority of such alterations indicate to the disorganizations in neuron-neuron communications. After pretreatment with Myo-inositol, modifications were ob- served in a fewer numbers of pyramidal neurons and axo-dendritic synapses. The majority of such alterations were superficial and