Haydar Ali Erken

Orexins increase penicillin-induced epileptic activity.

Orexins have been implicated with physiological function including sleep-wake cycle, energy homeostasis, drinking behavior, analgesia, attention, learning and memory but their effects on excitability are controversial. We investigated the effects of intracortical injections of orexin A (100 pmol) and B (100 pmol) on the electrophysiological manifestation of epileptic seizures induced by cortical penicillin application in adult male rats. In comparison to saline, orexin A and B enhanced significantly the spike number, spike amplitude and spectral power values induced by cortical penicillin. Our findings indicates that orexins enhances the hyperexcitable and hypersyncronic cortical epileptic activity induced by focal application of penicillin-G.

Orexins cause epileptic activity.

Orexins have been implicated in the regulation of sleep-wake cycle, energy homeostasis, drinking behavior, analgesia, attention, learning and memory but their effects on epileptic activity are controversial. We investigated whether intracortical injections of orexin A (100 pmol) and B (100 pmol) cause epileptic activity in rats. We observed epileptic seizure findings on these two groups rats. Orexin A and B also significantly increased total EEG power spectrum. Our findings indicate that orexins cause epileptic activity.

The effects of human umbilical cord blood transplantation in rats with experimentally induced spinal cord injury.

OBJECT Even though there have been many efforts to recover neuronal dysfunction following spinal cord injuries, there are limitations to the treatment of these injuries. The purpose of this laboratory investigation was to determine the clinical and neurophysiological effects of human umbilical cord blood (HUCB) transplantation in a rat hemisection model of spinal cord injury. METHODS In this study, experimental hemisection of the thoracic spinal cord was performed in rats. The rats were divided into 4 groups (6 rats in each group). One group of rats (Group 1) underwent thoracic laminectomy only. Rats in Group 2 underwent laminectomy and right hemisection of the thoracic spinal cord. Rats in Group 3 underwent right hemisection and implantation of freshly obtained HUCB on Day 0 postinjury. Rats in Group 4 underwent hemisection and implantation of freshly obtained HUCB on Day 4 postinjury. Clinical evaluations of rat motor function included the following: neurological examination, Rotarod performance, and inclined plane tests. Rats also underwent reflex evaluation. RESULTS The neurological examinations revealed that the frequency of plegic rats was 70.8% at the beginning of the study across all 4 groups; this value decreased to 20.8% by the end of the study. The percentage of rats with a normal examination increased from 25% to 50%. The results of Rotarod performance and 8-week inclined plane performance tests showed statistical significance (p < 0.05) in an overall group comparison across all time points. At the end of the 8 weeks, a statistically significant difference was found in the inclined plane test results between rats in Groups 1 and 2. There were no statistically significant differences between Groups 1, 3, and 4 (p < 0.05). When the reflex responses of the hemisectioned sides were compared, statistically significant differences were detected between groups (p < 0.05). All groups were significantly different with regard to the right-side reflex response score (p < 0.05). Spinal cord preparations of rats in all groups were examined for histopathological changes. CONCLUSIONS Human umbilical cord blood is stem cell rich and easily available, and it carries less risk of inducing a graft-versus-host reaction in the recipient. Human umbilical cord blood serum is also noted to contain stem cell–promoting factors, which is why cell isolation was not used in this study. Freshly obtained cord blood was also used because storage of cord blood has been reported to have some negative effects on stem cells. Transplantation of freshly obtained HUCB into the hemisectioned spinal cord experimental model demonstrated clinical and neurophysiological improvement.

Selenium partially prevents cisplatin-induced neurotoxicity: A preliminary study

Cisplatin is an anticancer drug and it has neurotoxic effects. On the other hand, the neuroprotective effect of selenium was observed in previous studies. However, the effect of selenium on cisplatin-induced neurotoxicity has not been studied yet. Therefore, we aimed to investigate whether selenium prevent cisplatin-induced neurotoxicity. Twenty-one male Wistar albino rats were divided into three groups: control (C), cisplatin (CS), cisplatin and selenium (CSE, n=7 in each group). Cisplatin (12 mg/kg/day, i.p.) was administered for 3 days to CS and CSE groups. Also, CSE group received via oral gavage 3 mg/kg/day (twice-a-day as 1.5 mg/kg) selenium 5 days before of cisplatin injection and continued for 11 consecutive days. The same volumes of saline were intraperitoneally and orally administered to C group at same time. At the end of experimental protocol, electrophysiological and histopathological examinations were performed. The nerve conduction velocity, amplitude of compound action potential and number of axon of CS group were significantly lower than the C group. However, the same parameters of CSE group were significantly higher than the CS group. Although, cisplatin has a peripheral neurotoxic effect in rats, this effect was partially prevented by selenium treatment. Thus, it appears that co-administration of selenium and cisplatin may be a useful approach to decrease severity of peripheral neurotoxicity.

Is rosuvastatin protective against on noise-induced oxidative stress in rat serum?

Noise, one of the main components of modern society, has become an important environmental problem. Noise is not only an irritating sound, but also a stress factor leading to serious health problems. In this study, we have investigated possible effects of rosuvastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, thought to have an antioxidant effect, on noise-induced oxidative stress in the serum of rat models. Thirty-two male Wistar albino rats were used. In order to ease their adaptation, 2 weeks before the experiment, the rats were divided into four groups (with eight rats per each group): Noise exposure plus rosuvastatin usage, only noise exposure, only rosuvastatin usage and control. After the data had been collected, oxidant (Malondialdehyde, nitric oxide [NO], protein carbonyl [PC]) and antioxidant (superoxide dismutase [SOD], glutathione peroxidase [GSH-PX], catalase [CAT]) parameters were analyzed in the serum. Results indicated that SOD values were found to be significantly lower, while PC values in serum were remarkably higher in the group that was exposed to only noise. GSH-Px values in serum dramatically increased in the group on which only rosuvastatin was used. During noise exposure, the use of rosuvastatin caused significantly increased CAT values, whereas it resulted in reduced PC and NO values in serum. In conclusion, our data show that noise exposure leads to oxidative stress in rat serum; however, rosuvastatin therapy decreases the oxidative stress caused by noise exposure.

Ozone partially prevents diabetic neuropathy in rats.

Neuropathy is one of the most common complications of diabetes mellitus. Although the beneficial effects of good blood glucose control on diabetic neuropathy are known, this control cannot completely prevent the occurrence and progression of diabetic neuropathy. The aim of this study was to investigate whether ozone prevents diabetic neuropathy. 36 adult female Sprague-Dawley rats were randomly divided into 6 groups (n=6): control (C), ozone (O), diabetic (D), ozone-treated diabetic (DO), insulin-treated diabetic (DI), and ozone- and insulin-treated diabetic (DOI). Diabetes was induced by a single injection of streptozotocin (60 mg/kg, intraperitoneal [i.p.]), after which insulin was administered (3 IU, i.p.) to the DI and DOI groups for 28 days, and 1.1 mg/kg (50 µg/ml) ozone was given to the O, DO, and DOI groups for 15 days. 4 weeks after the induction of diabetes, the nerve conduction velocity (NCV), amplitude of the compound action potential (CAP), total oxidant status (TOS), and total antioxidant status (TAS) were measured, and the oxidative stress index (OSI) was calculated. The NCV, amplitude of CAP, and TAS of the DI and DOI groups were higher than those of the D group; the amplitudes of CAP and TAS of the DO group were higher than those of the D group; and the TOS and OSI of the DO, DI, and DOI groups were lower than those of the D group. These findings indicate that ozone partially prevents diabetic neuropathy in rats. It appears that the preventive effects of ozone are mediated through oxidant/antioxidant mechanisms.

Blood Pressure Measurement in Freely Moving Rats by the Tail Cuff Method

Inconsistency in consecutive blood pressure values is one of the most frequently observed problems in tail cuff method. The aim of this study was to measure blood pressure using the tail cuff method in rats without heating, anesthesia, and movement restriction. In this study, it has been shown that blood pressure measurement could be obtained without problem using the tail cuff method in freely moving rats in their cage environment. Also, the reliability of consecutive blood pressure values obtained from freely moving rats was higher than ether anesthesia and restricted groups.

Boric acid reduces axonal and myelin damage in experimental sciatic nerve injury

The aim of this study was to investigate the effects of boric acid in experimental acute sciatic nerve injury. Twenty-eight adult male rats were randomly divided into four equal groups (n = 7): control (C), boric acid (BA), sciatic nerve injury (I) , and sciatic nerve injury + boric acid treatment (BAI). Sciatic nerve injury was generated using a Yasargil aneurysm clip in the groups I and BAI. Boric acid was given four times at 100 mg/kg to rats in the groups BA and BAI after injury (by gavage at 0, 24, 48 and 72 hours) but no injury was made in the group BA. In vivo electrophysiological tests were performed at the end of the day 4 and sciatic nerve tissue samples were taken for histopathological examination. The amplitude of compound action potential, the nerve conduction velocity and the number of axons were significantly lower and the myelin structure was found to be broken in group I compared with those in groups C and BA. However, the amplitude of the compound action potential, the nerve conduction velocity and the number of axons were significantly greater in group BAI than in group I. Moreover, myelin injury was significantly milder and the intensity of nuclear factor kappa B immunostaining was significantly weaker in group BAI than in group I. The results of this study show that administration of boric acid at 100 mg/kg after sciatic nerve injury in rats markedly reduces myelin and axonal injury and improves the electrophysiological function of injured sciatic nerve possibly through alleviating oxidative stress reactions.

Comparison of pre-treatment and post-treatment use of selenium in retinal ischemia reperfusion injury

AIM To investigate the effects of selenium in rat retinal ischemia reperfusion (IR) model and compare pre-treatment and post-treatment use. METHODS Selenium pre-treatment group (n=8) was treated with intraperitoneal (i.p.) selenium 0.5 mg/kg for 7d and terminated 24h after the IR injury. Selenium post-treatment group (n=8) was treated with i.p. selenium 0.5 mg/kg for 7d after the IR injury with termination at the end of the 7d period. Sham group (n=8) received i.p. saline injections identical to the selenium volume for 7d with termination 24h after the IR injury. Control group (n=8) received no intervention. Main outcome measures were retina superoxide dismutase (SOD), glutathione (GSH), total antioxidant status (TAS), malondialdehyde (MDA), DNA fragmentation levels, and immunohistological apoptosis evaluation. RESULTS Compared to the Sham group, selenium pre-treatment had a statistical difference in all parameters except SOD. Post-treatment selenium also resulted in statistical differences in all parameters except the MDA levels. When comparing selenium groups, the pre-treatment selenium group had a statistically higher success in reduction of markers of cell damage such as MDA and DNA fragmentation. In contrast, the post-selenium treatment group had resulted in statistically higher levels of GSH. Histologically both selenium groups succeeded to limit retinal thickening and apoptosis. Pre-treatment use was statistically more successful in decreasing apoptosis in ganglion cell layer compared to post-treatment use. CONCLUSION Selenium was successful in retinal protection in IR injuries. Pre-treatment efficacy was superior in terms of prevention of tissue damage and apoptosis.

Exercise and DHA Prevent the Negative Effects of Hypoxia on EEG and Nerve Conduction Velocity

It is known that hypoxia has a negative effect on nervous system functions, but exercise and DHA (docosahexaenoic acid) have positive effect. In this study, it was investigated whether exercise and/or DHA can prevent the effects of hypoxia on EEG and nerve conduction velocity (NCV). 35 adult Wistar albino male rats were divided into five groups (n=7): control (C), hypoxia (H), hypoxia and exercise (HE), hypoxia and DHA (HD), and hypoxia and exercise and DHA (HED) groups. During the 28-day hypoxia exposure, the HE and HED groups of rats were exercised (0% incline, 30 m/min speed, 20 min/day, 5 days a week). In addition, DHA (36 mg/kg/day) was given by oral gavage to rats in the HD and HED groups. While EEG records were taken before and after the experimental period, NCV records were taken after the experimental period from anesthetized rats. Data were analyzed by paired t-test, one-way ANOVA, and post hoc Tukey test. In this study, it was shown that exposure to hypoxia decreased theta activity and NCV, but exercise and DHA reduced the delta activity, while theta, alpha, beta activities, and NCV were increased. These results have shown that the effects of hypoxia exposure on EEG and NCV can be prevented by exercise and/or DHA.