Navegando por Palavras-chave "Motor behavior"

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    Lactulose decreases neuronal activation and attenuates motor behavioral deficits in hyperammonemic rats
    (Springer/Plenum Publishers, 2017) Mendes, Natalia Ferreira [UNIFESP]; Mariotti, Flora Franca Nogueira [UNIFESP]; Andrade, José Simões de [UNIFESP]; Viana, Milena de Barros [UNIFESP]; Céspedes, Isabel Cristina [UNIFESP]; Nagaoka, Márcia Regina [UNIFESP]; Le Sueur-Maluf, Luciana [UNIFESP]
    Lactulose is a nonabsorbable disaccharide commonly used in clinical practice to treat hepatic encephalopathy. However, its effects on neuropsychiatric disorders and motor behavior have not been fully elucidated. Male Wistar rats were bile-duct ligated, and 3 weeks after surgery, treated with lactulose administrated by gavage (1.43 or 3.57 g/kg), once a day for seven days. Plasma levels of ammonia, aspartate aminotransferase, total bilirubin, and creatinine were quantified and histopathological analysis of the livers was performed. Locomotor activity measurements were performed in an open field. The expression of water channel aquaporin-4 was investigated and the analysis of Fos protein immunoreactivity was used to evaluate the pattern of neural activation in brain areas related to motor behavior. Bile-duct ligated rats showed hyperammonemia, loss of liver integrity and function, impaired locomotor activity, reduced aquaporin-4 protein expression, and neuronal hyperactivity. Lactulose treatment was able to reduce ammonia plasma levels, despite not having an effect on biochemical parameters of liver function, such as aspartate aminotransferase activity and total bilirubin levels, or on the cirrhotic hepatic architecture. Lactulose was also able to reduce the locomotor activity impairments and to mitigate or reverse most changes in neuronal activation. Lactulose had no effect on reduced aquaporin-4 protein expression. Our findings confirm the effectiveness of lactulose in reducing hyperammonemia and neuronal hyperactivity in brain areas related to motor behavior, reinforcing the importance of its clinical use in the treatment of the symptoms of cirrhosis-associated encephalopathy.
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    Sleep deprivation abolishes the locomotor stimulant effect of ethanol in mice
    (Elsevier B.V., 2006-04-14) Araujo, Nilza Pereira de [UNIFESP]; Andersen, Monica Levy [UNIFESP]; Abilio, Vanessa Costhek [UNIFESP]; Gomes, Daniele Crespo [UNIFESP]; Carvalho, Rita de Cassia [UNIFESP]; Silva, Regina Helena da [UNIFESP]; Ribeiro, Rosana de Alencar [UNIFESP]; Tufik, Sergio [UNIFESP]; Frussa-Filho, Roberto [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The present study aimed to investigate the effects of sleep deprivation (SD) on the dose-dependent stimulant effect of ethanol (ETOH) on the open-field behavior of female and male mice. Sleep-deprived (48 h, multiple platforms method) or home-cage control female mice were treated with saline (SAL) or 1.4, 1.8 or 2.2 g/kg ETOH 5 min before behavioral testing. ETOH produced a dose-dependent increase in open-field locomotor behavior. This locomotor stimulant effect did not reflect a general stimulation in motor activity, since it was accompanied by a simultaneous decrease in rearing frequency as well as by no modification in immobility duration. the effects of ETOH on these three behavioral parameters were specifically modified by SD: the locomotor stimulant effect was abolished, the rearing inhibitory effect was potentiated and the lack of effect on immobility was changed to increase in immobility. Similar results were obtained for male mice although the effects of SD had a lower magnitude. the present findings demonstrate that the acute effect of ETOH on mice's motor activity are behaviorally complex and can be specifically modulated by SD. (c) 2006 Elsevier Inc. All rights reserved.