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31St International Epilepsy Congress Istanbul, Turkey 5Th – 9Th September 2015 ABSTRACTS 31st International Epilepsy Congress Istanbul, Turkey 5th – 9th September 2015 Epilepsia, 56(Suppl. 1):3–263, 2015 doi: 10.1111/epi.13241 Platform Session: Basic Science 0002 Sunday, 6th September 2015 MORPHOLOGICAL CHANGES IN EEG, AQUAPORIN- 4, C-FOS AND THE HIPPOCAMPUS OF ANIMAL 0001 MODELS WITH TEMPORAL LOBE EPILEPSY SODIUM SELENATE RETARDS EPILEPTOGENESIS INDUCED BY KAINIC ACID ı † † † ‡ VIA ACTIVATING PROTEIN PHOSPHATASE 2A E. Taskiran*,C.Ylmaz , N. Orhan , M. Bahceci , M. Kaya , B. Ahishali‡, M. Kucuk†, N. Arican‡, C. Gurses§ P. Zheng*, S. Liu*, N. Jones*, S. Shultz*, G. Dezsi*, D. Wright†, *Neurology Department, Istanbul Medipol University, Istanbul, C. Hovens‡, T.J. O’Brien*,§ † *The Royal Melbourne Hospital, Medicine, Melbourne, Turkey, Istanbul University, Research Institute of Experimental Medicine, Istanbul, Turkey, ‡Istanbul University Istanbul Australia, †The Florey Institutes of Neuroscience and Mental Faculty of Medicine, Istanbul, Turkey, §Department of Health, Melbourne, Australia, ‡The Royal Melbourne Hospital, Surgery, Melbourne, Australia, §Melbourne Brain Centre, Neurology and Clinical Neurophysiology, Istanbul University, Neurology, Melbourne, Australia Istanbul Faculty of Medicine, Istanbul, Turkey Purpose: Temporal lobe epilepsy (TLE) is the most frequent type of Purpose: Epileptogenesis describes the neurobiological processes that localization-related focal epilepsy seen in humans. It has a frequency rate convert a healthy brain into an epileptic brain. There are no treatments of 30–35% among all epilepsies, and comprises 70% of intractable available to mitigate epileptogenesis in clinical practice. Down-regula- epilepsies. With hippocampal sclerosis as the most often observed tion of protein phosphatase 2A (PP2A) activity increases phosphorylated histopathological finding, its epileptogenesis is still researched. tau (p-tau), which is implicated in acquired epilepsy. To investigate the role of PP2A in epileptogenesis, and the effects of a specific PP2A activa- – – Method: We investigated alterations in EEG findings during epilepto- tor sodium selenate we utilized three well-characterised rat models of genesis, and the immunohistochemical correlation of AQP4 and c-fos epilepsy: electrical amygdala kindling, post-kainic acid status epilepticus levels to hippocampal morphology in TLE induced by kainic acid (KA) (post-SE) and post-traumatic epilepsy (PTE). models. Sixty four young adult (220–270 gr) Wistar albino rats were divided into EEG and immunohistochemistry subgroups of sham, acute Method: For amygdala kindling, rats were implanted with subcuta- and chronic KA groups. Following the implantation of depth electrodes, neous osmotic pumps that delivered selenate (1 mg/kg/day) or vehicle rats were administered 5–15 mg/kg KA. In addition to observing AQP4 continuously for 4 weeks. Rats received 30 electrical stimulations over and c-fos proteins at the end of the first 24 hours and 60th day, continu- the final 3 weeks of treatment. For post-SE experiments, SE was ous video EEG monitoring (VEM) was carried out for 60 days. Seizure induced by kainic acid injections. Rats were then implanted with sub- patterns and interictal (II) epileptiform activities on VEM were investi- cutaneous osmotic pumps that continuously released selenate or vehicle gated. for 8 weeks. After 5 weeks of treatment, rats underwent MRI followed by continuous video-EEG monitoring. Rats were then given a drug Results: All rats in the acute KA group had status epilepticus (SE). washout period and then underwent additional video-EEG monitoring. While no spontaneous convulsive seizures were observed in the chronic For PTE, rats randomly suffered sham surgery or lateral fluid percus- KA group, electrophysiologically rhythmic slow waves were seen during sion injury and saline vehicle or selenate treatment. After 3-month the clinical staring episodes. Interictally, spike/sharp waves were recovery, all rats underwent video-EEG monitoring during and after observed. II activity tended to increase gradually during the 60 days. As the treatment. c-fos immune dying intensified in the hippocampal CA1 and amygdala, an increased rate of AQP4 immune dying in the endotelial cells in the Results: PP2A activity and expression of the PR55 regulatory subunit B brain capilleries (in the endotelial cells as well as the cytoplasma and feet were significantly decreased, and phosphorylation of tau was increased, of the astrocytes) were observed. We determined a correlation between in all three models. Selenate treatment slowed the progression of epilep- the increased intensity of c-fos and AQP4 proteins in hippocampus and togenesis in three models (delayed kindling and reduced spontaneous sei- amygdala with the electrophysiological finding of increased number of zures post-SE and PTE), reversed the biochemical abnormalities, and spikes. reduced hippocampal atrophy in the post-SE model. In post-SE and PTE model, this effect was sustained after drug washout, which indicated an Conclusion: Based on our findings, it is possible to suggest that impaired anti-epileptogenic effect. blood brain barrier (BBB) and increased AQP4 immunoreactivity contibute to the development of epileptogenesis. Conclusion: Epileptogenesis is associated with down-regulation of PP2A activity and an increase in phosphorylated tau, and enhancing PP2A activity with selenate is a potential anti-epileptogenic therapy. 3 4 Abstracts 0003 prevent the emergence of epilepsy following brain injury. Evidence has SHARED PATHOPHYSIOLOGY OF TEMPORAL LOBE emerged that microRNAs, a family of small non-coding RNAs, are ’ – important regulators of gene expression in epilepsy. Recent work showed EPILEPSY AND ALZHEIMER S DISEASE A that miRNA-134 is overexpressed in the temporal lobe of patients with DIFFERENTIAL PROTEOMICS APPROACH IN A pharmacoresistant seizures and in experimental models of epilepsy. POST-STATUS EPILEPTICUS MODEL Silencing miR-134 using intracerebroventricular injections of antago- E.-L. von Rüden*, C. Zellinger*, A. Walker*, V. Russmann*, mirs (Ant) potently suppressed evoked and spontaneous seizures in mice. K.J. Kleinwort†, C.M. Szober†, C. von Toerne‡, C.A. Deeg†, Here we explored a more clinically relevant route of delivery of these ‡ macromolecules, timing injection of antagomirs with blood-brain barrier S.M. Hauck , H. Potschka* (BBB) opening after status epilepticus in mice. *Ludwig-Maximilians-University, Inst. of Pharmacology, Toxicology, and Pharmacy, Munich, Germany, †Ludwig- Method: Status epilepticus (SE) was induced in C57BL/6 adult mice by Maximilians-University, Inst. of Animal Physiology, Munich, an intra-amygdala microinjection of kainic acid. Timing of BBB opening ‡ was assessed by Evans blue and FITC-dextran injections, and confirmed Germany, Helmholtz Center Munich, Research Unit Protein by extravasation of serum albumin and mouse IgG levels into the brain Science, Munich, Germany parenchyma. Antagomirs were locked nucleic acid- and cholesterol-mod- ified. Injections were then timed accordingly and mice subject to continu- Introduction: Clinical evidence points to a bidirectional link between ous long-term video-telemetry EEG recording. temporal lobe epilepsy (TLE) and Alzheimer’s disease (AD). However, clear-cut conclusions about a functional link between the pathophysiolo- Results: BBB opening in this model was apparent 2 h after status epilep- gies are clinically difficult. Therefore, we performed a large-scale differ- ticus. Systemic injection of Ant-134 at this time point did not alter the ential protome analysis in a rat TLE model of epileptogenesis and duration or severity of status epilepticus in mice but significantly reduced compared these data sets with available information about differential the number of spontaneous seizures recorded in mice compared with protein expression in AD models. scrambled-sequence and vehicle-injected status epilepticus controls. These seizure-suppressive effects persisted at 1 and 2 months after the Materials and Methods: Following an electrically-induced status SE. epilepticus in female Sprague Dawley rats, hippocampal (HC) and parahippocampal cortex (PHC) tissues were individually subjected to a Conclusion: The present study provides evidence that macromolecule label-free liquid chromatography tandem mass spectrometry analysis at targeting of an epilepsy-associated microRNA is effective using a clini- = three time points reflecting the early insult phase (2 days, n 5), latency cally-relevant delivery route, supporting the potential translation of this = phase (10 days, n 5), and the chronic phase with spontaneous recurrent anti-epileptogenic treatment for epilepsy. seizures (8 weeks, n = 5). Control animals (n = 5 per timepoint) were handled in parallel. Results: We identified proteins associated with amyloid-beta process- ing, deposition, plaque formation, and amyloid-beta-associated pathol- Platform Session: Drug Therapy ogy (ApoE and a-synuclein) being regulated in the time course of epileptogenesis. Sunday, 6th September 2015 Moreover, the analysis pointed to an epileptogenesis-associated down-regulation of the microtubule-associated protein Tau in the PHC, 0006 whereas Tau exhibited an up-regulation in the HC in the latency phase. ASSESSING BIOEQUIVALENCE OF GENERIC Furthermore, our data sets reveal a prominent dysregulation of mito- chondrial expression patterns, which is a typical feature of AD patho- MODIFIED RELEASE ANTIEPILEPSY DRUGS physiology, in the PHC and a less pronounced dysregulation in the
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