S258 P.1.g. Basic and clinical neuroscience − Neuropharmacology

Table 1 (abstract P.1.g.092).

NaCl PCP NaCl-H PCP-H NaCl-C PCP-C

BMD (mg/cm2)Male 143.2±5.2 139.1±4.2* 135.8±6.7** 132.9±8.4*** 142.4±9.2 134.1±5.7***Female 130.2±1.3 131.6±3.9 127.5±5.3 126.2±5.1 131.7±4.7 131±2.3

BMC (mg/cm)Male 7.6±0.5 6.9±0.5*** 6.8±0.5*** 6.2±0.7*** 7.2±0.7 6.7±0.6***Female 5.7±0.05 5.42±0.2** 5.3±0.4* 5.02±0.2*** 5.8±0.4 5.4±0.2**

Total fat (g)Male 100.5±12.1 93.2±7.9 83.5±14.3** 81.4±12.5*** 99.7±15.5 91.1±10.5*Female 78.9±4 71±7.2* 75±11.6 64.8±8** 81.2±5.4 71.9±6.2*Lean (g)Male 310.9±19.2 258±19*** 249.6±28.2*** 225.4±29.3*** 261.9±35.9*** 245.7±23.1***Female 168.3±10.1 163±6.6 146.3±7.4** 147.4±6.2** 161±9.6 160.7±8.7

*p< 0.05; **p< 0.01; ***p< 0.001 − comparing to control group.

[2] Moriarty, P.J., Lieber, D., Bennett, A., White, L., Parrella, M., Har-vey, P.D., Davis, K.L., 2001. Gender differences in poor outcomepatients with lifelong schizophrenia. Schizophr. Bull. 27, 103–113.

[3] Petronijevic, N., Sopta, J., Doknic, M., Radonjic, N., Petronijevic, M.,Pekic, S., Maric, N., Jasovic-Gasic, M., Popovic, V., 2013. Chronicrisperidone exposure does not show any evidence of bone mass deteri-oration in animal model of schizophrenia. Prog NeuropsychopharmacolBiol Psychiatry 46, 58−63.

P.1.g.093 Effects of ketamine in acute and repeated

dose on hippocampal theta waves in rats

M.C.A. Patrocınio1 °, L.R.L. Sampaio2, L.T.N. Borges2,L.R.C. Martins2, S.D. Nascimento2, T.M. Barbosa2,L.J.R. Farias2, J.M.F. Silva2, O.C. Vale3, S.M.M. Vasconcelos31Christus Medicine College, Pharmacology, Fortaleza, Brazil;2Federal University of Ceara, Department of Physiology andPharmacology, Fortaleza, Brazil; 3Federal University of Ceara,Department of Neurology, Fortaleza, Brazil

Purpose: Schizophrenia is a thought disorder that is character-ized by a disorganization of mental processes, thereby makingit a challenging and complex psychiatric disorder, leading theindividual to present multiple symptoms [1]. Ketamine (Ket) isa non-competitive N-methyl-D-aspartic acid (NMDA) receptorantagonist and infusions of ketamine in healthy individuals mayresult in cognitive and behavioral disturbances that are consistentwith the symptoms of schizophrenia [2]. Therefore, the analysisof the electroencephalogram (EEG) in ketamine model of schizo-phrenia could be a useful tool to investigate the brain mechanismsunderlying this disease [3], once the EEG is a representationof cerebral electrical activity. The objective was to investigatethe effects of ketamine in repeated doses of 10 and 50mg/kgin the theta waves hippocampal in pharmacological model ofschizophrenia in rats.

Methods: We used 18 male Wistar rats (200–300 g) that weredivided into three groups of six animals: G0 (treated with saline),G1 (treated with 10mg/kg of ketamine) and G2 (treated with50mg/kg of ketamine). The animals underwent a stereotacticsurgery for the implantation of electrode in the right hippocampusand, after three days, were treated for 5 consecutive days withbrainwave capture on the 1st and 5th days of treatment. Foracquisition and analysis of data EEG, the LabChart 8 Add-Onsversion 8.0 was used. Statistical analysis of all data from experi-ments was performed using the program GraphPad Prism 5 Demo

by one-way analysis of variance (ANOVA). When appropriate,comparisons between treatment groups and controls were made,using the Bonferroni post hoc test. The differences between groupswith p< 0.05 and lower were considered significant and the resultswere presented as mean±SEM.

Results: From the statistical analysis, it was observed thatacute administration of ketamine at a dose of 10mg/kg promotedsignificant changes in the average spectral power of theta bandin fifth (control: 4.71±0.34; ket 10: 4.38±0.21), tenth (control:4.71±0.34; ket 10: 4.38±0.21), fifteenth (control: 4.71±0.34;ket 10: 4 38±0.21) and twenty minutes (control: 4.71±0.34;ket 10: 4.38±0.21). Already in repeated doses for five days, itwas found that ket 10 caused significant changes in the averagespectral power in the theta band fifth (control: 3.99±0.09; ket 10:4.28±0.10), eleventh (control: 4.00±0.03; ket 10: 4.39±0.10),fifteenth (control: 4.01±0.05; ket 10: 4.36±0.04) and twentyminutes (control: 4.00±0.03; ket 10: 4.33±0.04).

Conclusion: Our results show that treatment with ketamine inrats exhibited changes in average spectral power on hippocampaltheta waves in rats, based on this study, some changes in EEG byketamine administration, which will serve as a basis for researchstudies of schizophrenia.

References

[1] Anticevic, A., Cole, M.W., Repovs, G., Savic, A., Driesen, N.R.,Yang, G., Cho, Y.T., Murray, J.D., Glahn D.C., Wang, X.J., Ktrys-tal, J.H., 2014 Connectivity, pharmacology, and computation: towarda mechanistic understanding of neural system dysfunction in schizo-phrenia. Front Psychiatry 4, 169.

[2] Dawson, N., McDonald, M., Higham, D.J., Morris, B.J., Pratt, J.A., 2014Subanesthetic Ketamine Treatment Promotes Abnormal Interactionsbetween Neural Subsystems and Alters the Properties of FunctionalBrain Networks. Neuropsychopharmacology 2014–2026.

[3] Hiyoshi, T., Hikichi H., Karasawa J.I., Chaki S., 2014. Metabotropicglutamate receptors regulate cortical gamma hyperactivities elicited byketamine in rats. Neurosci Lett. 224–229.

Disclosure statement: Acknowledgments: CNPq, CAPES, FUNCAP −Brazil.