ABSTRACT
Background: Many recent epidemiological studies have shown that epileptic patients are more likely suffer from depression, anxiety, and irritability. However, the cellular mechanisms of epilepsy-induced psychotic behaviors are not fully elucidated. Neurotrophin receptors have been suggested to be involved in epilepsy and also in psychiatric disorders. Up-regulation of p75NTR expression and activation of p75NTR signalling cascades after the seizure have been shown, but the role of the p75 receptor in epilepsy-induced psychotic behaviors has not been documented so far. Therefore, the present work aimed to investigate the effect of p75 receptor blockade on seizure activity, irritability, and anxiety-like behaviors in a rat model of status epilepticus
Methods: Rats were injected with pilocarpine [350 mg/ kg, i.p.] to induce status epilepticus. Then various behavioral tests were performed after the blockade of p75NTR alone or in combination with p75 antagonist and phenobarbital. Molecular analysis by PCR was performed to investigate the expression of p75 and pro-NGF
Results: Molecular findings indicated a high level of mRNA expression for both p75 receptors and pro-NGF in the epileptic model group. Results also showed that the administration of p75 antagonist alone or in combination with phenobarbital was able to significantly influence the behavioral responses. Furthermore, 20-hours video monitoring showed a decrease in the frequency and duration of seizures in the rat group receiving p75 antagonist
Conclusion: Taken together, the present study suggests that the blockade of the p75 receptor may affect the irritability and anxietyrelated behavior in a rat model of status epilepticus
ABSTRACT
Introduction: Transforming Growth Factor-Beta 1 [TGF-beta1] is a pleiotropic cytokine with potent anti-inflammatory property, which has been considered as an essential risk factor in the inflammatory process of Ischemic Stroke [IS], by involving in the pathophysiological progression of hypertension, atherosclerosis, and lipid metabolisms. -509C/T TGF-beta1 gene polymorphism has been found to be associated with the risk of IS. The aim of this meta-analysis was to provide a relatively comprehensive account of the relation between -509C/T gene polymorphisms of TGF-beta1 and susceptibility to IS
Methods: Male Wistar rats were divided into sham [receiving phosphate buffered saline within dorsal hippocampus], pilocarpine [epileptic model of TLE], single injection BDNF [epileptic rats which received single high dose of BDBF within dorsal hippocampus], and multiple injections BDNF [epileptic rats which received BDNF in days 10, 11, 12, and 13 after induction of TLE] groups. Their electrocorticogram was recorded and amplitude, frequency, and duration of spikes were evaluated
Results: Amplitude and frequency of epileptiform burst discharges were significantly decreased in animals treated with BDNF compared to pilocarpine group
Conclusion: Our findings suggested that BDNF may modulate the epileptic activity in the animal model of TLE. In addition, it may have therapeutic effect for epilepsy. More studies are necessary to clarify the exact mechanisms of BDNF effects
Subject(s)
Animals, Laboratory , Rats, Wistar , Polymorphism, Genetic , Stroke , Brain-Derived Neurotrophic Factor , Transforming Growth Factor beta1ABSTRACT
The seladin-1 [selective Alzheimer disease indicator-1], also known as DHCR24, is a gene found to be down-regulated in brain region affected by Alzheimer disease [AD]. Whereas, hair follicle stem cells [HFSC], which are affected in with neurogenic potential, it might to hypothesize that this multipotent cell compartment is the predominant source of seladin-1. Our aim was to evaluate seladin-1 gene expression in hair follicle stem cells. In this study, bulge area of male Wistar rat HFSC were cultured and then characterized with Seladin-1 immunocytochemistry and flow cytometry on days 8 to 14. Next, 9-11-day cells were evaluated for seladin-1 gene expression by real-time PCR. Our results indicated that expression of the seladin-1 gene [DHCR24] on days 9, 10, and 11 may contribute to the development of HFSC. However, the expression of this gene on day 11 was more than day 10 and on 10th day was more than day 9. Also, we assessed HFSC on day 14 and demonstrated these cells were positive for beta-? tubulin, and seladin-1 was not expressed in this day. HFSC express seladin-1 and this result demonstrates that these cells might be used to cell therapy for AD in future