Effects of probiotics on GABA/glutamate and oxidative stress in PTZ- induced acute seizure model in rats.

Studies conducted in recent years have indicated a relationship between epilepsy and gut microbiota. Ion channels, excitatory/inhibitory balance and regulatory systems play a role in the pathophysiology of epilepsy. In addition, gut dysbiosis is also involved in the pathophysiology of epilepsy. This research investigated the impacts of probiotic mixture on epileptic seizures, Gamma aminobutyric acid (GABA), glutamate, and TAS and TOS levels in hippocampal tissue in the PTZ-induced acute seizure model in rats. Four groups were formed with male Wistar albino rats. The first and second groups were given 1 ml/day saline solution, and the other groups were given 0.05 mg/1 ml/day vehicle or 109cfu/1 ml/day probiotic supplementation, respectively via gavage for 21 days. A single-dose PTZ (45 mg/kg) was administered to induce seizure. The stages of seizure were analyzed according to the Racine scale. While ELISA was used to determine GABA and glutamate levels in the hippocampus, an automated colorimetric method was utilized to measure oxidant/antioxidant biomarkers. It was found that by delaying the first myoclonic jerk (FMJ), and the onset of the generalized tonic-clonic seizures, the probiotic mixture demonstrated anticonvulsant effects against seizures. The probiotic mixture was found to increase the inhibitory neurotransmitter GABA. It was also found to decrease TOS levels and increase TAS concentration. The findings of this study showed that probiotic mixture reduced oxidative stress with its positive effects against PTZ-induced epileptic seizures. Further studies are needed to reveal potentially related mechanisms.

FGF-18 alleviates memory impairments and neuropathological changes in a rat model of Alzheimer's disease.

Alzheimer's disease (AD) is a multifactorial pathology marked by amyloid beta (Aß) accumulation, tau hyperphosphorylation, and progressive cognitive decline. Previous studies show that fibroblast growth factor 18 (FGF18) exerts a neuroprotective effect in experimental models of neurodegeneration; however, how it affects AD pathology remains unknown. This study aimed to ascertain the impact of FGF18 on the behavioral and neuropathological changes in the rat model of sporadic AD induced by intracerebroventricular (ICV) injection of streptozotocin (STZ). The rats were treated with FGF18 (0.94 and 1.88 pmol, ICV) on the 15th day after STZ injection. Their cognitive function was assessed in the Morris water maze and passive avoidance tests for 5 days from the 16th to the 21st days. Aß levels and histological signs of neurotoxicity were detected using the enzyme-linked immunosorbent assay (ELISA) assay and histopathological analysis of the brain, respectively. FGF18 mildly ameliorated the STZ-induced cognitive impairment; the Aß accumulation was reduced; and the neuronal damage including pyknosis and apoptosis was alleviated in the rat brain. This study highlights the promising therapeutic potential for FGF18 in managing AD.