Detection results of mitochondrial ΔΨm revealed a significant reduction 1.5, 3 and 12 h after convulsion in hippocampal neurons of experimental rats, which reached the trough at 12 h, and rapidly increased after 24 h. The expression of Mfn2 mRNA in the RS group was significantly lower than that in the control group, while the expression of Drp1 mRNA in RS group was distinctly higher than that in the control group.
Two weeks after KA-induced seizures, CCR2 deficiency not only reduced neuronal loss, but also attenuated seizure-induced behavioral impairments, including anxiety, memory decline, and recurrent seizure severity.
Abnormal expressions of sodium channel SCN1A and SCN3A genes alter neural excitability that are believed to contribute to the pathogenesis of epilepsy, a long-term risk of recurrent seizures.
Inhibition of SALM3 by SALM3 shRNA inhibited status epilepticus in the acute stage of disease and decreased spontaneous recurrent seizures in the Lithium-pilocarpine model of chronic stages of epilepsy.
Abnormal expressions of sodium channel SCN1A and SCN3A genes alter neural excitability that are believed to contribute to the pathogenesis of epilepsy, a long-term risk of recurrent seizures.
We have found that the KD increases brain PPARγ and that inhibition or genetic loss of PPARγ prevents the antiseizure effects of the KD on (1) acutely induced seizures in nonepileptic mice and (2) spontaneous recurrent seizures in epileptic mice.
Over 60 years after the initial description of PDE, we report the first animal model for this disease: an aldh7a1-null zebrafish (<i>Danio rerio</i>) displaying deficient lysine metabolism and spontaneous and recurrent seizures in the larval stage (10 days postfertilization).
Diplotype analysis of GABRA1 variants revealed association of rs12658835;rs7735530 (AG/AG) (P-valuecorrected = 0.034, OR = 3.75, 95% CI = 1.36-11.05) and rs12658835;rs7735530;rs7732641;rs2279020 (AGCA/AGCA) (P-valuecorrected = 0.035, OR = 2.48, 95% CI = 0.96-6.41) with recurrent seizures.
The differential expression of multiple genes in the PI3K-AKT signaling pathway in type II focal cortical dysplasia may be an important molecular mechanism underlying histological changes and recurrent seizures.
The differential expression of multiple genes in the PI3K-AKT signaling pathway in type II focal cortical dysplasia may be an important molecular mechanism underlying histological changes and recurrent seizures.
In addition, 30 min after intrahippocampal injection of 4-aminopyridine, IL-1β increased the incidence of SE, while IL-1RA prolonged the intervals between recurrent seizures.
The differential expression of multiple genes in the PI3K-AKT signaling pathway in type II focal cortical dysplasia may be an important molecular mechanism underlying histological changes and recurrent seizures.
The differential expression of multiple genes in the PI3K-AKT signaling pathway in type II focal cortical dysplasia may be an important molecular mechanism underlying histological changes and recurrent seizures.
And that VMAT2 protein transiently increased in acute stages (1 day and 3 days) after epileptic seizures in pilocarpine-treated rats; however, it clearly decreased after spontaneous recurrent seizures (7 days, 21 days, and 60 days after seizures).
This observation confirms the possibility that SCN5A mutations may confer susceptibility for recurrent seizure activity, supporting the emerging concept of a genetically determined cardiocerebral channelopathy.
From the data in GS, CT and TT genotype carriers of the MDR1 gene and TT genotype carriers of the GABRG2 gene had more recurrent seizures compared with others.
We demonstrate in wild-type mice that viral overexpression of ADK within astrocytes is sufficient to trigger spontaneous recurrent seizures in the absence of any other epileptogenic event, whereas ADK downregulation via AAV8-mediated RNA interference almost completely abolished spontaneous recurrent seizures in Adk-tg mice.
Mice heterozygous for a novel spontaneous Dnm1 mutation--fitful--experience recurrent seizures, and homozygotes have more debilitating, often lethal seizures in addition to severe ataxia and neurosensory deficits.
Like noncardiac organ phenotypes observed in other LQTS-susceptibility genes such as KCNQ1/deafness and SCN5A/gastrointestinal symptoms, this novel LQT2-epilepsy association raises the possibility that LQT2-causing perturbations in the KCNH2-encoded potassium channel may confer susceptibility for recurrent seizure activity.
Upregulation of EAAT3/EAAC1 in hippocampal and neocortical epilepsy may be an important modulator of extracellular glutamate concentrations and may occur as a response to recurrent seizures in these cell types.