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Review of studies that have used knockout mice to assess normal function of prion protein under immunological or pathophysiological stress
Abstract Deletion of cellular isoform of prion protein (PrPC) increases neuronal predisposition to damage by modulating apoptosis and the negative consequences of oxidative stress. In vivo studies have demonstrated that PrPC‐deficient mice are more prone to seizure, depression, and induction of epilepsy and experience extensive cerebral damage following ischemic challenge or viral infection. In addition, adenovirus‐mediated overexpression of PrPC reduces brain damage in rat models of cerebral ischemia. In experimental autoimmune encephalomyelitis, PrPC‐deficient mice reportedly have a more aggressive disease onset an...
Source: Microbiology and Immunology - July 8, 2014 Category: Microbiology Authors: Takashi Onodera, Akikazu Sakudo, Hirokazu Tsubone, Shigeyoshi Itohara Tags: Review Source Type: research

Studies for normal function of prion protein using knockout mice under the immunological or pathophysiological stress
ABSTRACT Deletion of cellular isoform of prion protein (PrPC) increased neuronal predisposition to damage by modulating to apoptosis, and the negative consequences to oxidative stress. In vivo studies demonstrated that PrPC‐deficient mice were more prone to seizure, depression and epilepsy induction, and exhibited an extent of the cerebral damage following an ischemic challenge or viral infection. Besides, adenovirus‐mediated PrPC over‐expression reduces brain damage in rat model of cerebral ischemia. In experimental autoimmune encephalomyelitis (EAE) PrPC‐deficient mice demonstrated more aggressive disease onset a...
Source: Microbiology and Immunology - May 1, 2014 Category: Microbiology Authors: Takashi Onodera, Akikazu Sakudo, Hirokazu Tsubone, Shigeyoshi Itohara Tags: Review Source Type: research

Effects of Brain IKKβ Gene Silencing by Small Interfering RNA on P-Glycoprotein Expression and Brain Damage in the Rat Kainic Acid-Induced Seizure Model.
Abstract Multidrug resistance mediated by over-expression of P-glycoprotein (P-gp) in brain is an important mechanism accounting for the drug-therapy failure in epilepsy. Over-expression of P-gp in epilepsy rat brain may be regulated by inflammation and nuclear factor-kappa B (NF-κB) activation. Inhibitory κB kinase subunit β (IKKβ) is an up-stream molecular controlling NF-κB activation. With the small interfering RNA (siRNA) technique and kainic acid (KA)-induced rat epileptic seizure model, the present study was aimed to further evaluate the role of NF-κB inhibition, via blocking IKKβ gene transcription, ...
Source: CNS and Neurological Disorders Drug Targets - August 27, 2013 Category: Drugs & Pharmacology Authors: Yu N, Liu H, Zhang YF, Su LY, Liu XH, Li LC, Hao JB, Huang XJ, Di Q Tags: CNS Neurol Disord Drug Targets Source Type: research

Transport of gabapentin by LAT1 (SLC7A5).
Abstract Gabapentin is used in the treatment of epilepsy and neuropathic pain. Gabapentin has high and saturable permeability across the BBB, but no mechanistic studies underpinning this process have been reported. The aim of the current study was to investigate the transport of gabapentin in a model of the BBB, identify the important drug transporter(s) and to use mathematical modelling to quantify the processes involved. A human brain endothelial cell line (hCMEC/D3) was utilised as an in-vitro model of the BBB. Uptake of radiolabeled gabapentin into cells in the presence of chemical inhibitors, siRNA or overexp...
Source: Biochemical Pharmacology - May 25, 2013 Category: Drugs & Pharmacology Authors: Dickens D, Webb SD, Antonyuk S, Giannoudis A, Owen A, Rädisch S, Hasnain SS, Pirmohamed M Tags: Biochem Pharmacol Source Type: research

Focal Scn1a knockdown induces cognitive impairment without seizures.
Abstract Cognitive impairment is a common comorbidity in pediatric epilepsy that can severely affect quality of life. In many cases, antiepileptic treatments fail to improve cognition. Therefore, a fundamental question is whether underlying brain abnormalities may contribute to cognitive impairment through mechanisms independent of seizures. Here, we examined the possible effects on cognition of Na(v)1.1 down-regulation, a sodium channel principally involved in Dravet syndrome but also implicated in other cognitive disorders, including autism and Alzheimer's disease. Using an siRNA approach to knockdown Na(v)1.1 s...
Source: Neurobiology of Disease - January 11, 2013 Category: Neurology Authors: Bender AC, Natola H, Holmes GL, Scott RC, Lenck-Santini PP Tags: Neurobiol Dis Source Type: research

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