Nonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti‐inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to the control group. NP (100 mg/kg/day) was administered to the NP and NP + TQ groups for 21 days. TQ (5 mg/kg/day) was administered to the NP + TQ and TQ groups for 7 after 21 days. At the end of the experiment, the new object recognition test was applied to the rats and the rats were killed and their brain tissues were removed. Sections taken from brain tissues were stained with hematoxylin–eosin for histopathological evaluation. In addition, neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), Cas‐3, and nerve growth factor (NGF) immunoreactivities were evaluated in brain tissue sections. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were determined. Comet assay was applied to determine DNA damage in cells. The results of our study showed that NP, caused behavioral disorders and damage to the cerebral cortex in rats. This damage in the form of neuron degeneration seen in the cortex was associated with apoptosis involving Cas‐3 activation, increased DNA damage, and free oxygen radicals. NP, SOD, and CAT caused a decrease in enzyme activities. In addition, the cellular protein NeuN was decreased, astrocytosis‐associated GFAP was increased, and growth factor NGF was decreased. When all our evaluations are taken together, treatment with TQ showed an ameliorative effect on the behavioral impairment and brain damage caused by NP exposure.

This study was aimed at examining the epileptiform activity of the 5-HT₂ serotonin receptor agonist and antagonist, and 5-hydroxytryptophan (5-HTP) in penicillin-induced epilepsy in albino Wistar rats. For this purpose, 90 albino male Wistar rats were used in this study. Epileptiform activity was induced by an injection of penicillin, an agonist of GABAA receptor, (500 IU, ic) into the somatomotor cortex. Thirty minutes after the injection of penicillin, 2,5-dimethoxy-4-iodoamphetamine (DOI, an agonist of 5-HT₂ receptor) (0.5, 1, 2 and 4 mg/kg, ip), methysergide, an antagonist of 5-HT₂ receptor, (1, 10, 20, 50 and 100 µM, icv) and 5-HTP, precursor of 5-HT, (25, 50, 75 and 100 mg/kg, ip) were administered, respectively. DOI, at the doses of 1 and 2 mg/kg, significantly decreased penicillin-induced epileptiform activity (p < 0.05). Methysergide, at the doses of 20, 50 and 100 µM, significantly increased the mean spike frequency of penicillin-induced epileptiform activity (p < 0.05). The doses of 50, 75 and 100 mg/kg of 5-HTP decreased the mean spike frequency of penicillin-induced epileptiform activity (p < 0.05). The mean of amplitude of penicillin-induced epileptiform activity did not significantly change in any of the groups (p > 0.05). The electrophysiological data from the present study suggest that serotonin 5-HT₂ receptors have an important role in controlling penicillin-induced epileptiform activity in the rat.

Objective. This study aimed to examine the effects of vortioxetine, a novel antidepressant, on epileptiform activity in pentylenetetrazole (PTZ)-induced kindling model in rats. Methods. For this purpose, 20 male Wistar Albino rats were used, and epileptiform activity was induced by injection of PTZ (35 mg/kg, i.p., three times a week). In the vortioxetine groups, vortioxetine (5 mg/kg and 10 mg/kg) was administered before the kindling process. During the kindling process, the Fisher and Kittner seizure scales were used to score seizure severity. After kindling, novel object recognition (NOR) tests were performed to evaluate the cognitive performance of rats. Electrodes were implanted into the fully kindled animals for ECoG recordings. Results. In the PTZ group, the number of total spikes was 13671136 spikes/20 minutes. First myoclonic jerks decreased while seizure severity and total spike count increased in the PTZ group. On the other hand, the total spike number and seizure severity significantly decreased and first myoclonic jerks increased in the vortioxetine groups compared to the PTZ group. Based on the NOR test, vortioxetine administration markedly raised the discrimination index compared to the PTZ group. Significance. Electrophysiological and behavioural data from the present study suggest that vortioxetine, a novel drug, plays a critical role in controlling PTZ-induced epileptiform activity in rats. Vortioxetine may therefore be a valuable candidate to prevent seizure activity and treat cognitive deficits associated with epilepsy.