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Neuroscience. 2014 Feb 14;259:223-31. doi: 10.1016/j.neuroscience.2013.11.049. Epub 2013 Dec 4.

Omega-3 prevents behavior response and brain oxidative damage in the ketamine model of schizophrenia.

Author information

1
Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil; Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM), Porto Alegre, RS, Brazil. Electronic address: alz@unesc.net.
2
Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
3
Laboratório de Psiquiatria Molecular, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
4
Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil; Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM), Porto Alegre, RS, Brazil.
5
Laboratório de Psiquiatria Molecular, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil; Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM), Porto Alegre, RS, Brazil.

Abstract

Supplementation with omega-3 has been identified as an adjunctive alternative for the treatment of psychiatric disorders, in order to minimize symptoms. Considering the lack of understanding concerning the pathophysiology of schizophrenia, the present study hypothesized that omega 3 prevents the onset of symptoms similar to schizophrenia in young Wistar rats submitted to ketamine treatment. Moreover, the role of oxidative stress in this model was assessed. Omega-3 (0.8g/kg) or vehicle was given by orogastric gavage once daily. Both treatments were performed during 21days, starting at the 30th day of life in young rats. After 14days of treatment with omega-3 or vehicle, a concomitant treatment with saline or ketamine (25mg/kg ip daily) was started and maintained until the last day of the experiment. We evaluated the pre-pulse inhibition of the startle reflex, activity of antioxidant systems and damage to proteins and lipids. Our results demonstrate that supplementation of omega-3 prevented: decreased inhibition of startle reflex, damage to lipids in the hippocampus and striatum and damage to proteins in the prefrontal cortex. Furthermore, these changes are associated with decreased GPx in brain tissues evaluated. Together, our results suggest the prophylactic role of omega-3 against the outcome of symptoms associated with schizophrenia.

KEYWORDS:

ANOVA; BDNF; Brain-derived neurotrophic factor; CAT; DHA; DNPH; EDTA; EPA; GPx; GSH; NADPH; PUFAs; ROS; SOD; TBARS; analysis of variance; antioxidants; catalase; dihydronicotinamide-adenine dinucleotide phosphate; dinitrophenylhydrazine; docosahexaenoic acid; eicosapentaenoic acid; ethylenediaminetetraacetic acid; glutathione; glutathione peroxidase; ketamine; omega 3; polyunsaturated fatty acids; prepulse inhibition; reactive oxygen species; schizophrenia; superoxide dismutase; thiobarbituric acid reactive species

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