171 resultados para EPILEPSY-PRONE RATS


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Wild running (WR) behavior of rats seen in response to intense acoustic stimulation of audiogenic seizure-paradigm is very similar to the panic flight and can be facilitated by subconvulsive doses of strychnine. The present work aimed to test whether antipanic procedures, such as dorsal periaqueductal gray (dPAG) lesion and imipramine treatments, affect the strychnine-facilitated WR. In study 1, six Wistar male adult rats with electrolytic lesion of dPAG had their WR completely blocked, whereas it was facilitated in 50% of sham-lesioned control rats by a dose of 0.5 mg/kg of strychnine administered intraperitoneal. This effect was not reproduced with a higher strychnine dose (1.0 mg/kg). In study 2, the effects of imipramine were investigated by testing 36 rats under a dose of strychnine that induces WR in 50% of subjects. They were assigned into three experimental groups: imipramine treatments of 5.0 and 10.0 mg/kg, and infusions of saline. All these treatments were subchronical with three intraperitoneal injections within 24h. Imipramine (10.0mg/kg) reduced the incidence of WR in comparison to the saline results. It is concluded that strychnine-facilitated WR is reduced by antipanic procedures and, therefore, can be viewed as a manifestation closely related to panic. (C) 2003 Elsevier B.V. B.V. All rights reserved.

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Sleep-deprived rats exhibit defensive fighting as well as explosive flights very similar to the wild-running of audiogenic seizures. In order to determine why sleep deprivation is a common factor that facilitates both panic and convulsive manifestations, the present study was undertaken to investigate whether rats that display sleep deprivation-induced fighting (SDIF) are the same as those that are susceptible to audiogenic wild-running (WR). Twenty-eight male adult Wistar rats were divided into two groups assigned to two e-sleep deprivation for 5 days and had their SDIF evaluated in social experimental schemes. In the first, 18 subjects were submitted to REM grouping. After 1 week for recovery, their susceptibility to WR was tested in an acoustic stimulation trial ( 104 dB, 200 Hz, 60 S). Rats that did not present WR received a lactate infusion and were tested again by acoustic stimulation 40 min later. In the second experimental scheme, 10 subjects were initially evaluated for WR susceptibility and the number of SDIF was recorded in social grouping after I week. Three categories of WR-susceptibility were determined: WR-sensitive rats, intermediate WR-sensitive rats and WR-insensitive rats. T'he number of SDIF in each category was significantly different and there was a high positive correlation (r=0.89; Spearman test) between the number of SDIF and the level of WR-susceptibility. We conclude that the reasons why sleep deprivation exerts facilitatory effects on both panic and convulsive manifestations are due to overlappings of neural pathways responsible for both behavioral patterns and for the property of sleep deprivation to increase neuronal excitability. (C) 2002 Elsevier B.V. B.V. All rights reserved.

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The effects of dexamethasone (Dex) on the metabolic parameters, peripheral insulin, and glucose sensitivity in vivo as well as on islet function ex vivo of rats submitted to low-protein diet were analyzed. Dexamethasone (1.0 mg/kg body weight) was administered intraperitoneally daily to adult Wistar rats fed on a normal-protein diet or low-protein diet (LPD) for 5 days, whereas control rats fed on a normal-protein diet or low-protein diet (LP) received saline alone. At the end of the experimental period, LP rats showed a significant reduction in serum insulin, total serum protein, and serum albumin levels compared with rats fed on a normal-protein diet (P < .05). All these parameters tended to be normalized in LPD rats (P < .05); furthermore, these rats exhibited increased serum glucose and nonesterified fatty acid levels compared with LP rats (P < .05). Rats submitted to the low-protein diet demonstrated normal peripheral glucose sensitivity and improved peripheral insulin sensitivity, which was reversed by Dex treatment. A reduced area of islets from LP rats was partially recovered in LPD rats (P < .05). At 16.7 mmol/L glucose, insulin secretion from LPD islets was also partially recovered and was significantly higher than that from LP islets (P < .05). In conclusion, induction of insulin resistance by Dex treatment reverses most of the metabolic alterations in rats submitted to a low-protein diet. In addition, several islet functions were also improved by Dex, confirming the plasticity of pancreatic islets in adverse conditions. (C) 2008 Elsevier B.V. All rights reserved.

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Objectives: We have analyzed the peripheral insulin and glucose sensitivity in vivo, and islet function ex vivo in rats with different degrees of insulin resistance induced by dexamethasone (DEX).Methods: Dexamethasone, in the concentrations of 0.1 (DEX 0.1), 0.5 (DEX 0.5), and 1.0 mg/kg body weight (DEX 1.0) was administered daily, intraperitoneally, to adult Wistar rats for 5 days, whereas controls received saline.Results: Dexamethasone treatment induced peripheral insulin resistance in a dose-dependent manner. At the end of the treatment, only DEX 1.0 rats showed significant increase of postabsorptive blood glucose and serum triglycerides, and nonesterified fatty acids levels. Incubation of pancreatic islets in increasing glucose concentrations (2.8-22 mM) led to an augmented insulin secretion in all DEX-treated rats. Leucine, carbachol, and high KCl concentrations induced the insulin release in DEX 0.5 and DEX 1.0, whereas arginine augmented secretion in all DEX-treated groups.Conclusions: We demonstrate that in DEX 0.5 and, especially in DEX 0.1 groups, but not in DEX 1.0, the adaptations that occurred in the endocrine pancreas are able to counteract metabolic disorders (glucose intolerance and dyslipidemia). These animal models seem to be interesting approaches for the study of degrees of subjacent effects that may mediate type 2 diabetes (DEX 1.0) and islet function alterations, without collateral effects (DEX 0.1 and DEX 0.5).

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