approved by the Research Ethics Committee of the Federal University of São Paulo (UNIFESP), number 0164/12. Results: The two-way ANOVA with repeated measures revealed significant effects of time [F (2,36) = 33.99, p b 0.001], prenatal treat- ment [F (1,36) = 4, 32 p b 0.05], and postnatal treatment [F (1,36) = 113.87, p b 0.001] and interaction prenatal treatment × postnatal treat- ment [F (1,36) = 5, 80, p b 0.05], time × postnatal treatment [F (2,36) = 33.54, p b 0.001], and prenatal treatment × postnatal treatment × time [F (2,36) = 3.28, p b 0.05]. Duncan's test revealed that the behavioral sensitization to AMP occurred in the 3rd day injection of SAL or AMP (5th day of treatment), with a significant increase in locomotion in the AMP-treated groups (3rd day N 1st day). Importantly, the prenatal treatment with POLY:IC potentiated behavioral sensitization to AMP. Discussion/conclusions: Our results indicate that prenatal POLY:IC administration potentiated AMP-induced behavioral sensitization and support the observation that patients with schizophrenia present an increase in the prevalence of substance use disorders. Acknowledgments/financial support: CAPES, FAPESP, CNPQ, and AFIP. doi:10.1016/j.yebeh.2014.08.042 010 — (BOR0176) PER2, PER3, and clock polymorphisms are not associated with juvenile myoclonic epilepsy in a sample of the Brazilian population J.P.L. Born a , B.P. Santos b , T.E.B.S. Marques b , M.V.S. Malta b , T.G. Andrade c , F.T. Gameleira d , L.L.G. Gitaí d , R. Secolin e , D.L.G. Gitaí b a Universidade Federal de Alagoas, Brazil b Setor de Genética e Biologia Molecular, ICBS, UFAL, Brazil c Campus Arapiraca, UFAL, Brazil d Setor de Neurologia, HUPAA, UFAL, Brazil e Department of Medical Genetics, Faculty of Medical Sciences, UNICAMP, São Paulo, Brazil Rationale: Juvenile myoclonic epilepsy (JME) is a subtype of common idiopathic generalized epilepsy (IGE) and accounts for 10% of all forms of epilepsy and up to 26% of IGE. Onset is at puberty with equal sex ratio, and it is characterized by myoclonic jerks, occasional generalized tonic– clonic seizures, and, sometimes, absence seizures. In JME, seizures occur predominantly after awakening in the morning. Despite the existence of rare mutations responsible for some familial forms inherited in a Mendelian pattern, the genetics of JME is complex and probably reflects the simultaneous involvement of multiple genes with minor effects and environmental factors. The identification of these susceptibility genes is a great challenge. For this purpose, genetic association studies directed to candidate genes according to their molecular function are an experi- mental approach that has been widely used. Because chronodependency and sleep deprivation are the major determinants of seizures in JME, we hypothesized that “Clock genes” could be associated with this epilepsy subtype. We performed this case/control study to evaluate whether the Per2 C111G, Clock T3111C, and Per3 VNTR SNPs might influence the risk of JME. These variants have been reported to be associated with diurnal preference sleep disturbances. In addition, a possible interaction between the three polymorphisms has been investigated. Methods: This study included 97 unrelated Brazilian patients with JME and 212 healthy control subjects. Diagnostic criteria of the Commission on Classification and Terminology of the International League against Epilepsy were used to diagnose probands with JME. Patients were matched with controls by age, sex, ethnicity, and geographic origin. Individuals with a history of epileptic seizures or neuropsychiatric disorders were excluded from the control sample. The polymorphisms were detected by PCR or PCR–RFLP methods. All descriptive and statistical analyses were performed using SNPstat software. Results: The genotype distribution did not deviate significantly from that expected by Hardy–Weinberg equilibrium, as estimated by the chi- square test. Replicated genotyping of 30% of the samples revealed 100% concordance. Genotype proportions and allele frequencies for the three polymorphisms did not differ significantly between the groups even when the OR was adjusted for the clinical variables. We also tested for interactions between polymorphisms. None of the combined Clock T3111C, Per2 C111G, or Per3 VNTR genotypes differed significantly between the groups. Discussion/conclusions: To our knowledge, this is the first association study of “Clock genes” polymorphisms (Clock T3111C, Per2 C111G, and Per3 VNTR) in JME. Our results suggest that none of the variants were related to JME susceptibility in the Brazilian population. Since these genes codify proteins that interact with each other, the combination of polymorphisms in different Clock genes could have a synergistic or inhibitory effect on susceptibility threshold. However, our study seems to exclude a possible relationship between these three SNPs and JME at least in the Brazilian population. Multicenter studies involving a large number of subjects will be required to more definitively reveal the contribution, if any, of these and other “Clock genes” variants in JME. Acknowledgments/financial support: UFAL, CAPES, CNPq, and FAPEAL. doi:10.1016/j.yebeh.2014.08.043 011 — (BRO0187) Electrographic patterns of spontaneous recurrent seizures in a focal model of temporal lobe epilepsy induced by continuous electrical stimulation of the perforant pathway A.C.S. Broggini, D.C. Wolf, I.M. Esteves, J.P. Leite Department of Neurosciences and Behavioral Sciences, University of São Paulo, Brazil Rationale: Patients with symptomatic epilepsy in general present electrographic abnormalities, such as increase of focal slow activity and interictal spikes. Electroencephalographic recording analyses allow the identification of changes of oscillatory frequencies and interictal spike patterns, which can be potentially useful tools in predicting seizures. Our objective was to characterize the spontaneous recurrent seizures (SRSs) and perform the spectral analysis of local field potential (LFP) segments before and after seizures detected in a temporal lobe epilepsy (TLE) model induced by continuous and focal electrical stimulation of the perforant pathway (PP) with activity onset restricted to the hippocampus. Methods: Freely-moving awake male Wistar rats received PP stimula- tion (frequency of 20 Hz for 10 s) within 8 h. Seizures were monitored by video-EEG, 6 h per day and 6 days per week over 75 days. The LFPs were recorded in the dentate gyrus (DG) of the hippocampus and medial prefrontal cortex (mPFC). For the spectral analysis, 20-minute segments before and after seizures were analyzed. The power spectrum was calculated using the mtspectrumc script of Chronux (software package of MATLAB routines) and was performed for the following six frequency bands: delta (0.5–4 Hz), theta (5–10 Hz), beta (10–15 Hz), low gamma (LG, 30–55 Hz), high gamma (HG, 65–100 Hz), and high frequency oscillations (HFO, 150–200 Hz). Results: In this model, 68 SRSs were observed. Of a total of 16 stimulated animals, 8 had at least one electrographic seizure predominantly in the afternoon. The mean latency of the first SRSs was 37 days. The spectral analysis of the preictal and the postictal recording showed that slow activities and HFOs were increased and that HG band decreased compared with baseline in preictal segments of both mPFC and hippocampus regions. However, power in LG frequency presented different patterns of activity in these regions before onset of SRSs. There was a reduction in LG energy relative to the baseline in the hippocampus, Abstracts 185