The effects of regular swimming exercise during sodium valproate treatment on seizure behaviors and EEG recordings in pentylenetetrazole-kindled rats

We investigated the effects of alone/combined regular swimming exercise and sodium valproate on epileptic seizure behaviors and EEG recordings, anti-oxidative mechanism, learning, and memory in pentylenetetrazole (PTZ)-kindled rats. Forty-eight healthy rats were randomly divided into eight equal groups as control (CONT), swimming exercise (EX), sodium valproate (SV), SV+EX, PTZ, EX+PTZ, SV+PTZ and SV+EX+PTZ. The rats were forced to regular swimming exercise for 60 min every other day, 13 doses of PTZ (40 mg/kg) were given to induce epileptic seizures and 200 mg/kg SV was given for 28 days. Epileptic seizures were evaluated by visual observation and EEG recordings (total spike numbers and number of epileptiform discharges). Memory and learning skills were assessed with passive avoidance test. According to our visual seizure observations, seizure latency was prolonged only in SV+EX+PTZ (p < 0.001) group, seizure severity score decreased in SV+PTZ (p < 0.05) and SV+EX+PTZ (p < 0.001) groups and seizure frequency was reduced in SV+PTZ (p < 0,001), EX+PTZ (p < 0,001), and SV+EX+PTZ (p < 0,001) groups. Total spike numbers and number of epileptiform discharges highly increased in PTZ group, whereas they decreased in swimming exercise and/or SV treatment groups. The most effective result was seen in the combined therapy group. Memory deficit was observed in PTZ -kindling group, but it didn't change with exercise or SV. Based on our results, regular swimming exercise had positive effects on PTZ-induced seizure frequency, and combined therapy of regular swimming exercise and SV is the most effective way to ameliorate visual seizure behaviors and decrease spike numbers and number of epileptiform discharges according to EEG recordings. Regular swimming exercise could be an alternative option to reduce the dose of SV and the side effects of SV can be avoided in clinical aspects

The effects of atorvastatin on memory deficit and seizure susceptibility in pentylentetrazole-kindled rats

Deficits in memory function have been observed in pentylentetrazole (PTZ)-kindled rats. In the present study we examined the effects of atorvastatin ((3-hydroxy-3-methylglutaryl-coenzyme A [HMG-CoA] reductase inhibitor) on PTZ kindling and related memory deficits in rats trained with the passive avoidance test. Subconvulsive PTZ doses rendered a gradual increase in seizure activity. PTZ kindling caused long-term memory to deteriorate. Atorvastatin per se and in PTZ-kindled rats improved learning and memory functions. It also prolonged latency (time to appearance of spike potentials) and diminished the amplitude and frequency of spike potentials, which indicate epileptic discharges. These novel findings suggest that the favorable effect of the atorvastatin on memory deficits provoked by PTZ kindling might be of clinical utility. (C) 2010 Elsevier Inc. All rights reserved

Isolation of Shewanella putrefaciens from cultured european sea bass, (Dicentrarchus labrax) In Turkey

This study describes the etiological agent that caused mortalities on cultured European sea bass, Dicentrarchus labrax, L., in Turkey. The sick fish showed lethargy, loss of appetite, exophthalmus, and ulcers over the dorsal part of the body. Internally, liver haemorrhages, spleen enlargement (splenomegaly) were observed. The spleen, liver and kidney were pale. Ascites in the abdominal cavity was also observed. Gram-negative, cytochrome oxidase and catalase positive and H(2)S producing rods were isolated from skin ulcers, kidney, spleen, liver and blood and identified as Shewanella putrefaciens by using both standard methods and API 20 E test system. Histological examination of sea bass naturally infected with S. putrefaciens indicated depletion of white and red pulpas and deposition of haemosiderin in the melanomacrophage centres in the spleen. The kidney was severely affected, displaying necrosis in renal tubules. Intestinal mucosa membrane sloughed into the lumens. There were vacuole degeneration. necrotic areas in the fatty liver tissue

Effects of erythropoietin pretreatment on single dose pentylentetrazole-induced seizures in rats

Although it is accepted that prolonged and repeated seizures can cause epileptogenesis, memory deficits and neuronal death, the precise relation between epileptic seizures and neuronal death remains unclear. Erythropoietin (EPO) exhibits neuroprotective and anti-epileptic effects. We investigated the effect of a single pentylentetrazole (PTZ) induced tonic-clonic seizure on the pyramidal neurons of the cornu ammonis 1 (CA1) and CA3 regions of hippocampus. We also investigated the effects of EPO on seizure, memory and on brain-derived neurotrophic factor (BDNF), tyrosine receptor kinase-B, sirtuin-1 (SIRT1), which are important for memory. Forty male rats were divided into four groups: control, saline treated, single 60 mg/kg dose PTZ treated, 3000 IU/kg EPO treated, and 3000 IU/kg EPO treated 24 h before PTZ administration. Seizure latency and severity were assessed following PTZ injection. A passive avoidance test was performed 24 h after seizure. BDNF, TrkB and SIRT1 levels were measured in serum, hippocampus and cortex. The hippocampus was examined histologically, and neuronal nuclear antigen (NeuN) was investigated using immunohistochemistry. EPO pretreatment decreased seizure severity and prolonged seizure latency. Single dose PTZ-induced seizures did not affect memory. Numbers of cells in the CA1 region did not change, although the number of dark stained neuron increased. Both total cell numbers and percentage of dark stained cells were elevated in the CA3 region following PTZ induced seizures. EPO pretreatment decreased the number of dark cells in both CA1 and CA3 regions and the number of cells in the CA3 region. NeuN labeling was unchanged in the CA1 and CA3 regions in the PTZ group; however, EPO pretreatment increased NeuN labeling in the CA3 region. Although EPO exhibited an anticonvulsive effect, single dose EPO pretreatment did not affect memory in either animals not exposed to PTZ or animals that had been subjected to PTZ-induced seizures. EPO pretreatment prolonged seizure latency and reduced seizure severity after PTZ-induced seizures. The anti-seizure and neuroprotective effects of EPO pretreatment may be due to the protection of CA1 and CA3 neurons, possibly owing to SIRT1 and BDNF activity

Vanadyl sulfate protects against streptozotocin-induced morphological and biochemical changes in rat aorta

The aim of this study was to investigate the protective effects of vanadyl sulfate on aorta tissue of normal and streptozotocin (STZ)-induced diabetic rats, morphologically and biochemically. The animals were made diabetic by an intraperitoneal injection of streptozotocin (65 mg/kg) and vanadyl sulfate (100 mg/kg) that was given every day for 60 days by gavage technique to rats. Under the light and transmission electron microscopes, hypertrophy of the vessel wall, focal disruption in the elastic lamellae, an increase in thickness of total aortic wall, tunica intima, subendothelial space and adventitial layer, and a disorganization in smooth muscular cells of the tunica media were observed in diabetic animals. The aorta lipid peroxidation (LPO) levels were significantly increased and the aorta glutathione (GSH) levels were significantly reduced in STZ diabetic rats. In diabetic rats administered vanadyl sulfate for 60 days, aorta LPO levels significantly decreased and the aorta GSH level significantly increased. In conclusion, in vivo treatment with vanadyl sulfate of diabetic rats prevented the morphological and biochemical changes observed in thoracic aorta of diabetic animals. Copyright (K 2006 John Wiley & Sons, Ltd