seizure may occur after mild traumatic brain injury (tbi), and the severity of tbi can be considered the most crucial factor for an increased risk of recurring seizures as well as for the development of posttraumatic epilepsy. however, the effect of seizures in epileptogenesis after mild tbi cannot yet be accurately confirmed. this study was designed to determine whether mild tbi increases seiz...

introduction: since organophosphorus compounds (op) are toxic and designed to destroy insects and pest species, there are many hazards associated with their use. although, the main target site of these compounds is acetylcholinesterase (ache), however it has become increasingly evident that ops have also other direct effects on cellular processes. in the present study, the effects of low concen...

Seizure activity has been proposed to result in the generation of reactive oxygen species (ROS), which then contribute to seizure-induced neuronal damage and eventually cell death. Although the mechanisms of seizure-induced ROS generation are unclear, mitochondria and cellular calcium overload have been proposed to have a crucial role. We aim to determine the sources of seizure-induced ROS and ...

Traumatic brain injury is considered as one of the main causes of morbidity and mortality worldwide. Apart from primary mechanical injury, Secondary injuries due to inflammation and apoptosis result in great neuronal damage. Current treatments are not able to regenerate the damaged part and prevent future sequels. Using human stem cells with self-assembling scaffolds may be promising in treatme...

It is well established that brain blood barrier dysfunction following the onset of seizures may lead to serum albumin extravasation into the brain. However, the effect of albumin extravasation on the development of epilepsy is yet to be fully elucidated. Previous studies have predominantly focused on the effect of albumin absorption by astrocytes; however, the present study investigated the eff...

This study aims to explore the molecular mechanism of neuronal axonal lesions caused by high glucose, and investigate protective effect Lycium barbarum polysaccharide (LBP) on axon damage with in vitro models. A rat model type II diabetic encephalopathy was established, rats were treated LBP for 10 weeks. Morris water maze experiment used detect spatial learning memory ability. Neuronal measure...

Intracellular calcium increase is an early key event triggering ischemic neuronal cell damage. The role of T-type voltage-gated calcium channels in the neuronal response to ischemia, however, has never been studied. Using an in vitro model of ischemia-induced delayed cell death in rat organotypic hippocampal slice cultures, we show that T-type calcium channels inhibitors drastically reduce isch...

Background: Gap junctions composed of connexins (Cx) are functional in cell defense by propagation of toxic/death molecules to neighboring cells. Hippocampus, one of the brain regions with particular vulnerability to damage, has a wide network of gap junctions. Functional response of astrocytic Cx30 and neuronal Cx32 to hippocampal damage is unknown. Methods: We infused lipopolysaccharide (LPS)...

The Wld mouse mutant demonstrates a remarkable phenotype of delayed axonal and synaptic degeneration after nerve lesion. In this study, the authors tested the hypothesis that expression of Wld protein is neuroprotective in an in vivo mouse model of global cerebral ischemia. This model is associated with selective neuronal degeneration in specific brain regions such as the caudate nucleus and CA...

Chronic cerebral hypoperfusion (CCH), which induces oxidative stress and inflammation in the brain, has previously been associated with cognitive impairment and neuronal cell damage. Melatonin is a well-known free radical scavenger and antioxidant; therefore, the present study investigated the protective effects of melatonin against CCH-induced cognitive impairment and neuronal cell death in a ...