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The aim of the present study was to examine the effect of subchronic co-administration of folic acid (F) and L-arginine (A) on behavioural and electroencephalographic (EEG) characteristics of DL homocysteine thiolactone (H) induced seizures in adult rats. The activity of membrane ATPases in different brain regions were also investigated. Rats were treated with F, A, or vehicle for 15 days (regimen: F 5 mg/kg + A 500 mg/kg (F5A500); F 10 mg/kg + A 300 mg/kg (F10A300)). Seizures were elicited by convulsive dose of H (H, F5A500H, F10A300H) Subchronic supplementation with F and A did not affect seizure incidence, number of seizure episodes, and severity in F5A500H and F10A300H groups vs. H group. However, a tendency to increase latency and decrease the number of seizure episodes was noticed in the F10A300H group. EEG mean spectral power densities during ictal periods were significantly lower in F10A300H vs. H group. The activity of Na+/K+-ATPase and Mg2+-ATPase was significantly increased in almost all examined structures in rats treated with F and A. We can conclude that subchronic supplementation with folic acid and L-arginine has an antiepileptic effect in DL homocysteine thiolactone induced epilepsy.

Influence of folic acid on the CNS is still unclear. Folate has a neuroprotective effect, while on the other hand excess folate can exacerbate seizures in epileptics. The aim of the present study was to examine the effect of subchronic administration of folic acid on behavioural and electroencephalographic (EEG) characteristics of DL homocysteine thiolactone induced seizures in adult rats. The activity of Na+/K+-ATPase and Mg2+-ATPase in different brain regions was investigated. Adult male Wistar rats were divided into groups: 1. Controls (C, 0.9% NaCl); 2. DL homocysteine-thiolactone 8.0 mmol/kg (H); 3. Subchronic supplementation with folic acid 5 mg/kg for 7 days (F) and 4. Subchronic supplementation with F + single dose of H (FH). Seizure behaviour was assessed by incidence, latency, number and intensity of seizure episodes. Seizure severity was described by a descriptive scale with grades 0-4. For EEG recordings, three gold-plated recording electrodes were implanted into the skull. Subchronic supplementation with folic acid did not affect seizure incidence, median number of seizure episodes and severity in FH, comparison with H (p GT 0.05). The majority of seizure episodes in all groups were of grade 2. There were no significant differences in lethal outcomes at 24 h upon H injection in the FH vs. H group. The activity of Na+/K+-ATPase and Mg2+-ATPase was significantly increased in almost all examined structures in the FH vs. H group. Subchronic folic acid administration did not exacerbate H induced seizures and completely recovered the activity of ATPases.

The aim of the study was to examine the effects of chronic exercise training on seizures induced by homocysteine thiolactone (HCT) in adult rats. Rats were assigned to: sedentary control; exercise control; sedentary +HCT; exercise + HCT group. Animals in the exercise groups ran 30 min daily on a treadmill for 30 consecutive days (belt speed 20 m/min), while sedentary rats spent the same time on the treadmill (speed 0 m/min). On the 31st day, the HCT groups received HCT (8.0 mmol/kg), while the control groups received vehicle. Afterwards, convulsive behavior and EEG activity were registered. Lipid peroxidation, superoxide dismutase (SOD) and catalase (CAT) activity were ascertained in the rat hippocampus. No signs of seizures were registered in sedentary and exercise control rats. Seizure latency was increased, while number of seizure episodes and spike-and-wave discharges (SWD) in EEG were decreased in the exercise + HCT compared to the sedentary +HCT group. Seizure incidence, the severity thereof and duration of SWDs were not significantly different between these groups. Exercise partly prevented increase of lipid peroxidation and decrease of the SOD and CAT activity after HCT administration. These results indicate beneficial effects of exercise in model of HCT induced seizures in rats, what could be, at least in part, a consequence of improved antioxidant enzymes activity.

Epilepsija nastaje kao rezultat prevage ekscitatornih nad inhibitornim fenomenima u centralnom nervnom sistemu i jedno je od vodećih neuroloških oboljenja (1-2% u opštoj populaciji). Homocistein, zajedno sa svojim metabolitom homocistein tiolaktonom, je značajan faktor rizika za razvoj kardiovaskularnih i neuroloških oboljenja, uključujući epilepsiju. Jedini put produkcije tioaminokiseline homocisteina u organizmu je metabolizam metionina. Akutna administracija homocistein tiolaktona adultnim pacovima dovodi do elektroencefalogramske (EEG) epileptogene aktivnosti, konvulzivnog ponašanja, te predstavlja pogodan eksperimentalni model generalizovane epilepsije. Epilepsija je često praćena anksioznošću, koja je u pozitivnoj korelaciji sanivoom homocisteina prema rezultatima ATTICA studije, dok rezultati Hordaland studije negiraju ovu povezanost. Zbog dramatičnog toka epileptičnih napada i mogućnosti povređivanja, sedentaran način života je čest kod bolesnika sa epilepsijom. Poslednjih godina pojavili su se dokazi da fizička aktivnost može smanjiti intenzitet nekih tipova konvulzivnih napada, mada postoje rezultati koji ukazuju na pojačanje epileptiformne EEG aktivnosti nakon fizičke aktivnosti. Istraživanja ukazuju da se selektivnom deprivacijom REM (eng. rapid eye movement) spavanja redukuje nivo homocisteina kod pacova. Međutim, spavanje je fiziološki proces koji čini jednu trećinu ljudskog života i njegov nedostatak je povezan sa hiperekscitabilnošću. Azot monoksid (NO) pripada grupi gasnih neurotransmitera. Neuralna NO sintaza (nNOS) je prisutna u strukturama CNS u kojima NO kao neuromodulator reguliše ekscitabilnost. Međutim, povišena ekspresija inducibilne NOS (iNOS) pronađena je kod pacijenata sa epilepsijom..., Epilepsy is a result of an imbalance between inhibitory and excitatory phenomena in the central nervous system. It is one of the leading neurological disorders and affects 1-2% of the world's population. Homocysteine, together with its metabolite homocysteine thiolactone is a risk factor for numerous cardiovascular and neurological disorders, including epilepsy. Homocysteine is produced by metabolism of methionine. Systemic administration of homocysteine to adult rats significantly alters neuronal circuits, leading to specific epileptogenic activity in the electroencephalogram (EEG) with convulsive episodes in animal behavior. Therefore, it represents suitable experimental model of generalized epilepsy. Anxiety is а common comorbidity among epileptic patients. Results of ATTICA study showed positive correlation between homocysteine and anxiety, while results of Hordaland study did not show the existence of this relationship. Increased sedentary lifestyle among epileptic patients is observed in populationbased studies Physical activity can play a favorable role in reducing the frequency and intensity of some seizures. However, an exercise – induced increase of epileptiform EEG activity has been also reported. Recent studies have shown that REM sleep deprivation can lower plasma homocysteine levels. On the other hand, sleep is a cyclic and vital physiological process that constitutes one-third of human life and deprivation of sleep is associated with hyperexcitability. Nitric oxide (NO) is a member of gasotransmitter family. Neuronal NO synthase (nNOS) is expressed in various brain regions in which NO acts as modulator of excitability. However, inducible NOS (iNOS) is found to be overexpressed in brains of humans with epilepsy...

Thioacetamide (TAA) is widely used as a model of hepatic encephalopathy (HE). The aim of our study was to investigate the effects of TAA on electroencephalographic (EEG) changes in rats and to compare them with human HE. Male Wistar rats were divided into groups: (1) saline-treated group and (2) TAA-treated groups: TAA(300) (300 mg/kg), TAA(600) (600 mg/kg), and TAA(900) (900 mg/kg). Daily dose of TAA (300 mg/kg) was administered intraperitoneally once (TAA(300)), twice (TAA(600)), or thrice (TAA(900)) in subsequent days. EEG changes were recorded about 24 h after the last dose of TAA. Absolute and relative power density in alpha bands were significantly higher in TAA(300) versus control group. In TAA(300), absolute beta power density was higher and relative beta power density was lower versus control group. Absolute alpha, theta, delta, and relative theta power were significantly lower, while relative power in delta band was significantly higher in TAA(900) versus control group (p LT 0.01). In conclusion, decrease in EEG voltage with an increase in delta relative power, which correspond to the EEG manifestations of severe HE in humans, was observed in TAA(900) group. Electrical activity in TAA(300) group correlates with mild HE in humans.

Thioacetamide (TAA) is widely used as a model of hepatic encephalopathy (HE). The aim of our study was to investigate the effects of TAA on electroencephalographic (EEG) changes in rats and to compare them with human HE. Male Wistar rats were divided into groups: (1) saline-treated group and (2) TAA-treated groups: TAA(300) (300 mg/kg), TAA(600) (600 mg/kg), and TAA(900) (900 mg/kg). Daily dose of TAA (300 mg/kg) was administered intraperitoneally once (TAA(300)), twice (TAA(600)), or thrice (TAA(900)) in subsequent days. EEG changes were recorded about 24 h after the last dose of TAA. Absolute and relative power density in alpha bands were significantly higher in TAA(300) versus control group. In TAA(300), absolute beta power density was higher and relative beta power density was lower versus control group. Absolute alpha, theta, delta, and relative theta power were significantly lower, while relative power in delta band was significantly higher in TAA(900) versus control group (p LT 0.01). In conclusion, decrease in EEG voltage with an increase in delta relative power, which correspond to the EEG manifestations of severe HE in humans, was observed in TAA(900) group. Electrical activity in TAA(300) group correlates with mild HE in humans.

Thioacetamide (TAA) exerts hepatotoxic, neurotoxic and carcinogenic effects. The aim of our study was to investigate the effects of TAA on lipid peroxidation and catalase activity in various rat brain regions. Male Wistar rats were divided into following groups: 1. control, saline-treated; 2. thioacetamide-treated groups, TAA(300) (300 mg/kg), TAA(600) (600 mg/kg) and TAA(900) (900 mg/kg). Daily dose of TAA (300 mg/kg) was administered intraperitoneally once (TAA(300)), twice (TAA(600)) and three times (TAA(900)) in consecutive days. Brain samples were collected 24 h after the last dose of TAA and malondialdehyde (MDA) level and catalase activity were determined in cortex, brainstem and hippocampus. MDA level was significantly increased while catalase activity was significantly lower in all brain regions in TAA(900) group in comparison with control group. In TAA(600) MDA level was increased in the brainstem and cortex when compared to control (p LT 0.01). The same dose of TAA(600) mg/kg induced a significant decline in catalase activity in the brainstem and cortex and an increase in its activity in the hippocampus when compared to control (p LT 0.01). In TAA(300) an increase in MDA level was evident only in the brainstem. Catalase activity was significantly higher in the cortex and hippocampus in TAA(300) group in comparison with control (p LT 0.01). Based on these results, it may be concluded that various rat brain regions have different sensitivity to TAA-induced lipid peroxidation with hippocampus being less sensitive than cerebral cortex and brainstem.

The effects of ethanol on epilepsy are very complex. Ethanol can have depressant as well as excitatory effect on different animal models of epilepsy. Systemic administration of homocysteine can trigger seizures. The aim of the present study was to examine the changes of total spectral power density after ethanol alone and together with homocysteine thiolactone in adult rats. Adult male Wistar rats were divided into following groups: I. saline-injected, (control) C; 2. D, L-homocysteine thiolactone, H (8 mmol/kg); 3. ethanol, E (E(0.5), 0.5 g/kg; E(1), 1 g/kg; E(2), 2 g/kg) and 4. E (E(0.5), E(1), and E(2)) 30 min prior to H, EH (E(0.5)H, E(1)H and E(2)H). For EEG recordings three gold-plated screws were implanted into the skull. Our results demonstrate that ethanol, when applied alone, increased total EEG spectral power density of adult rats with a marked spectrum shift toward low frequency waves. In EH groups, increasing doses of ethanol exhibited a dose-dependent effect upon spectral power density. Ethanol increased EEG spectral power density in E(0.5)H and E(1)H group, comparing to the H group (p GT 0.05), the maximal increase was recorded with the lowest ethanol dose applied. The highest dose of ethanol (E(2)H) significantly decreased total power spectra density, comparing to the H group. We can conclude that high doses of ethanol depressed marked increase in EEG power spectrum induced by D,L-homocysteine thiolactone.