Cafer Marangoz

Evidence that sodium nitroprusside possesses anticonvulsant effects mediated through nitric oxide.

The effect of sodium nitroprusside (SNP) on epileptiform activity elicited by administration of penicillin (500 units) into the somatomotor cortex was studied in anaesthetized rats. No epileptiform activity was observed after intracortical microinjection of SNP (5 and 20 nM). Microinjection of penicillin into the somatomotor cortex induced epileptiform activity in electrocorticograms (ECoG). Epileptiform discharges elicited by penicillin were significantly decreased by SNP. The effect of SNP appeared within 1 min of application and lasted for 2-5 min. The inhibitory effect of SNP on epileptiform activity could be prevented by pretreatment with methylene blue (20 nM), a soluble guanylate cyclase inhibitor. Prior injection of haemoglobin (5 microliter), a nitric oxide (NO) scavenger, prevented the anticonvulsant effect of SNP. These results suggest that NO may be an endogenous anticonvulsant substance.

Anticonvulsant effects of melatonin on penicillin-induced epileptiform activity in rats

In the present study, we investigated the effects of melatonin on penicillin-induced epileptiform activity in female Wistar rats. The left cerebral cortex was exposed by craniotomy under urethane anesthesia for the induction of epilepsy by intracortical microinjection of penicillin (200 IU) into the left sensorimotor cortex. The epileptiform activity was analyzed by electrocorticogram (ECoG). Ten minutes before the penicillin injection, 20, 40 or 80 microg of melatonin was administered intracerebroventricularly and ECoG was monitored for 1 h. Forty or 80 microg of melatonin significantly increased the latency to epileptiform activity. Furthermore, melatonin significantly decreased the frequency of spike and spike-wave activity, whereas the amplitude of spikes remained unchanged. In conclusion, data obtained from the present study suggest that melatonin suppresses penicillin-induced epileptiform activity, and it may be an endogenous anticonvulsant.

Anticonvulsant effects of focal and intracerebroventricular adenosine on penicillin-induced epileptiform activity in rats

Adenosine has potent anticonvulsant effects on various models of experimental epilepsy. In the present study, we examined the effects of focal and intracerebroventricular (i.c.v.) adenosine on penicillin-induced epileptiform activity in Wistar rats. The effects of theophylline, a non-selective adenosine receptor antagonist, were also researched. The recordings of electrocorticogram (ECoG) were carried out by using a data acquisition system, under urethane anesthesia. Adenosine was given in doses of 1, 10 and 100 microg/rat via focal and i.c.v. 30 min after penicillin administration. Theophylline was injected in doses of 1, 10 and 100 microg/rat by i.c.v. too. Adenosine administration significantly decreased the spike frequency while theophylline increased. Focal adenosine is more effective than i.c.v. adenosine. 100 microg adenosine is an effective dose that causes a decrease in epileptiform activity during experiments. We also demonstrated that 100 microg theophylline significantly increased epileptiform activity. Our findings suggest that focal adenosine is more effective than i.c.v. adenosine on epileptiform activity.

Effects of nitric oxide on passive avoidance learning in rats

To investigate the effects of nitric oxide (NO) on passive avoidance learning, L-NAME, D-NAME, and L-arginine were administered i.p. 30 min prior to learning trial; the effects of these substances were tested 24 h later using a passive avoidance apparatus in rats. To reveal the effect of NO on consolidation of acquired memory, L-NAME, D-NAME, and L-arginine were administered i.p. immediately after learning trials and animals were tested 24 h later. Effect of NO on retention was also investigated by injecting L-NAME, D-NAME, and L-arginine (same dosages) 30 min prior to 24 h testing (retrieval). L-NAME administered 30 min before and 24 h after learning trial significantly decreased the avoidance latency but there was no significant effect on consolidation. L-Arginine appeared to enhance the retention of acquired memory significantly, whereas D-NAME had no effect on any testing regime. The results suggest that NO may be involved in learning and retention of passive avoidance

Nitric oxide synthase inhibitors protect cerebellar Purkinje cells from zinc-induced cell loss in adult rat

Zinc is an important trace element in biological systems; however, excessive extracellular zinc could lead to neuronal cell death following ischemia, seizures, and brain trauma. In this study, we investigated whether the intracortical injection of zinc sulphate (200 μg/kg, i.c.) changes total number of Purkinje cells in the cerebellum and whether different types nitric oxide synthase inhibitors, N-(G)-nitro-L-arginine methyl ester (L-NAME), N(omega)-nitro-L-arginine (L-NNA), aminoguanidine and 7-nitroindazole (7-NI), have protective effects against zinc neurotoxicity in Wistar albino rats. Animals were divided into 6 groups: control, zinc, zinc+L-NAME (100 mg/kg, i.p.), zinc+L-NNA (100 mg/kg, i.p.), zinc+7-NI (100 mg/kg, i.p.) and zinc+aminoguanidine (100 mg/kg, i.p.) groups. Total number of Purkinje cells in the cerebellum was estimated using unbiased stereological technique as 318,947 ± 20,549, 123,483 ± 23,762, 206,537 ± 43,128, 178,135 ± 26,635, 193,148 ± 46,104 and 212,910 ± 26,399 in the control, zinc, zinc+L-NAME, zinc+L-NNA, zinc+7-NI and zinc+aminoguanidine groups, respectively (mean ± SD). The number of Purkinje cells in zinc group was significantly lower than that of the other groups (P<0.001). It was found that the nitric oxide synthase inhibitors have neuroprotective effect against zinc neurotoxicity on Purkinje cells. These data show that the inhibition of the nitric oxide synthase could prevent some of the deleterious effects of zinc on Purkinje cells.

Do cochlear nuclei contribute to auditory lateralization? A stereological evaluation of neuron numbers.

The aim of this study was to estimate the total number of cells in the subdivisions of the cochlear nucleus (CN) of the rat with unbiased stereological methods. The total number of neurons was determined in both the ventral cochlear nucleus (VCN) and the dorsal cochlear nucleus (DCN) to compare the right and left sides. The total cell numbers were 15,280 in the left VCN, 15,400 in the right VCN, 10,260 in the left DCN, and 10,860 in the right DCN. Comparison of the right and left major subdivisions of the CN of the rat showed that there was no significant difference between the right and left sides of the rat CN. This result indicates that the CNs do not contribute to auditory lateralization in the rat in regard to cell numbers.

Protective effects of melatonin and omega-3 on the hippocampus and the cerebellum of adult Wistar albino rats exposed to electromagnetic fields

The purpose of the study was to investigate the effects of pulsed digital electromagnetic radiation emitted by mobile phones on the central nervous system of the adult Wistar albino rats. The study evaluated structural and functional impacts of four treatment arms: electromagnetic field (EMF) exposed; EMF exposed + melatonin treated group (EMF + Mel); EMF exposed + omega-3 (ω3) treated group (EMF + ω3); and control group (Cont). The 12-weeks-old rats were exposed to 900 MHz EMF for 60 min/day (4:00–5:00 p.m.) for 15 days. Stereological, biochemical and electrophysiological techniques were applied to evaluate protective effects of Mel and ω3. Significant cell loss in the CA1 and CA2 regions of hippocampus were observed in the EMF compared to other groups (p < 0.01). In the CA3 region of the EMF + ω3, a significant cell increase was found compared to other groups (p < 0.01). Granular cell loss was observed in the dentate gyrus of the EMF compared to the Cont (p < 0.01). EMF + ω3 has more granular cells in the cerebellum than the Cont, EMF + Mel (p < 0.01). Significant Purkinje cell loss was found in the cerebellum of EMF group compared to the other (p < 0.01). EMF + Mel and EMF + ω3 showed the same protection compared to the Cont (p > 0.05). The passive avoidance test showed that entrance latency into the dark compartment was significantly shorter in the EMF (p < 0.05). Additionally, EMF had a higher serum enzyme activity than the other groups (p < 0.01). In conclusion, our analyses confirm that EMF may lead to cellular damage in the hippocampus and the cerebellum, and that Mel and ω3 may have neuroprotective effects.

Effects of spermine and the passive avoidance learning (PAL) following cerebral ischemia in chicks: Association with neuroprotection of pyramidal cells

The aim of this study is to investigate the effects of spermine and the passive avoidance learning on hippocampus following transient cerebral ischemia in the chicks. The study is composed of the pure control (CG), sham (SG) and experimental groups (n=20). Experimental groups (ischemia group, IG and ischemia-spermine group, ISG) were exposed to ischemia for 20min whereas the SG was exposed to sham operation and CG group was not exposed to any operation. Passive avoidance learning (PAL) was applied to the half number of the subjects in each group. Both before and after 7days from the ischemia, operated animals were taken to PAL and then they were sacrificed. Total numbers of neurons in the hippocampus were stereologically estimated using Cresyl violet stained sections. We detected that number of neurons was increased following PAL and especially spermine treatment. According to our results, we suggested that spermine may reduce the deleterious effects of the ischemia by causing to increase in the neuronal number and so, it may be slightly supportive to the PAL.

Proconvulsant effect of papaverine on penicillin-induced epileptiform activity in rats

AIM Papaverine is a vasodilator agent that is an opium alkaloid. It exhibits its effects by inhibiting the phosphodiesterase enzyme. Papaverine administration is widely used to avoid symptomatic vasospasm after subarachnoid hemorrhage. We aimed, in this research, to study the effects of papaverine on the epileptic discharges stimulated by penicillin. MATERIAL AND METHODS Adult female Wistar rats (220±30 g) were included in this research (n=30). Rats were anesthetized with urethane (1.25 g/kg) and then the left cerebral cortex was reached by opening a burr hole with a drill. Penicillin G sodium salt (500 IU)(200 IU/1 μl) was injected into the left lateral ventricle to produce epileptiform activity. Thirty minutes before penicillin G sodium injection, papaverine was administered at doses of 5, 10, 20 or 40 mg/kg intraperitoneally. RESULTS There was no significant difference in spike frequency between the control group and the groups given 5 mg/kg, 10 mg/ kg or 40 mg/kg papaverine, while 20 mg/kg papaverine significantly increased the spike frequency (p < 0.05). CONCLUSION Papaverine augments the epileptiform activity produced by penicillin injection. It is important to remember that papaverine might induce convulsions in patients who have epilepsy. More research is required to understand the mechanisms of the proconvulsant influence of papaverine in epilepsy.