NMDA receptors are among the crucial elements of central nervous system models. Recent studies show that both conductance and kinetics of these receptors are changing voltage-dependently in some parts of the brain. Therefore, several models have been introduced to simulate their current. However, on the one hand, kinetic models-which are able to simulate these voltage-dependent phenomena-are computationally expensive for modeling of large neural networks. On the other hand, classic exponential models, which are computationally less expensive, are not able to simulate the voltage-dependency of these receptors, accurately. In this study, we have modified these classic models to endow them with the voltage-dependent conductance and time constants. Temperature sensitivity and desensitization of these receptors are also taken into account. We show that, it is possible to simulate the most important physiological aspects of NMDA receptor's behavior using only three to four differential equations, which is significantly smaller than the previous kinetic models. Consequently, it seems that our model is both fast and physiologically plausible and therefore is a suitable candidate for the modeling of large neural networks.

Male dysfunction is common in patients with temporal lobe epilepsy (TLE). We evaluated whether melatonin, as a supplement, can play a positive role in reducing the epileptogenesis imposing abnormalities of spermatozoa and testes in epileptic rats. Status epilepticus was induced based on the TLE lithium-pilocarpine model. Two patterns of melatonin were administered to the epileptic animals along the mean durations of latent (14 days) and chronic (60 days) phases. Sperm parameters, different antioxidant enzyme levels, germ cell apoptosis, body and relative sex organ weights were evaluated in all groups 60 days following SE induction. Chronic TLE caused a significant reduction in sperm parameters. In the testis, the reduced level of antioxidant enzymes was accompanied by a significant increase in malondialdehyde concentration. The presence of oxidant condition in the testes of epileptic animals caused expanded apoptosis in the germ cell layer. Moreover, the amount of weight gain in epileptic animals was more prominent. Melatonin administration was able to improve sperm motility by increasing the total antioxidant level. There was also a significant reduction in the spermatogenic cell line apoptosis and the extra weight gain of melatonin-treated animals. Melatonin supplementation might be considered as an acceptable cotreatment in epileptic patients.

Feature outcome of hippocampus and extra-hippocampal cortices was evaluated in melatonin treated lithium-pilocarpine epileptic rats during early and chronic phases of temporal lobe epilepsy (TLE). After status epilepticus (SE) induction, 5 and 20 mg/kg melatonin were administered for 14 days or 60 days. All animals were killed 60 days post SE induction and the histological features of the rosrto-caudal axis of the dorsal hippocampus, piriform and entorhinal cortices were evaluated utilizing Nissl, Timm, and synapsin I immunoflorescent staining. Melatonin (20 mg/kg) effect on CA1 and CA3 neurons showed a region-specific pattern along the rostro-caudal axis of the dorsal hippocampus. The number of counted granular cells by melatonin (20 mg/kg) treatment increased along the rostro-caudal axis of the dorsal hippocampus in comparison to the untreated epileptic group. The density of Timm granules in the inner molecular layer of the dentate gyrus decreased significantly in all melatonin treated groups in comparison to the untreated epileptic animals. The increased density of synapsin I immunoreactivity in the outer molecular layer of the dentate gyrus of untreated epileptic rats showed a profound decrease following melatonin treatment. There was no neuronal protection in the piriform and entorhinal cortices whatever the melatonin treatment. Long-term melatonin administration as a co-adjuvant probably could reduce the post-lesion histological consequences of TLE in a region-specific pattern along the rostro-caudal axis of the dorsal hippocampus.

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Both epilepsy and valproate (VPA), as an antiepileptic drug, negatively affect male sexual function. The present study was conducted to evaluate the ameliorating impacts of ginseng on sperm quality, architecture of seminiferous epithelium and spermatogenic cell apoptosis in temporal lobe epilepsy (TLE) animal model treated with VPA. Fifty-six adult male rats were divided into seven groups including untreated control (Co), epilepsy (E), valproate (V), epilepsy-valproate (EV), epilepsy-ginseng (EG), valproate-ginseng (VG) and epilepsy-valproate-ginseng (EVG). Animals received daily intraperitoneal injections of valproate and ginseng for 30 days. We observed a significant decline in bilateral testes' weight and sperm counts, along with reduction in normal morphology in the EV group. Ginseng sharply improved both sperm counts and spermatozoa with normal morphology in EVG animals. Although sperm motility decreased in V and EV groups, ginseng ameliorated sperm motility in VG and EVG animals. Besides, VPA sharply decreased spermatogenesis quality and increased germ cell apoptosis. Finally, ginseng significantly diminished apoptosis in VG rats and improved spermatogenesis in both VG and EVG groups. In conclusion, ginseng treatment has shown a positive impact on spermatogenesis and sperm quality in TLE rats treated with VPA. Therefore, it may be a beneficial adjuvant along with VPA treatment in the epileptic patient. K E Y W O R D S epilepsy, ginseng, rat, testis, valproate How to cite this article: Ganjkhani M, Nourozi S, Bigonah R, Rostami A, Shokri S. Ameliorating impacts of ginseng on the apoptosis of spermatogenic cells and sperm quality in temporal lobe epilepsy rat model treated with valproate.