Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of repetitive pilocarpine-induced status epilepticus (SE) in the hippocampal Na(+)/K(+)ATPase activity were studied in developing rat. Na(+)/K(+)ATPase is a membrane-bound enzyme responsible for the active transport of sodium and potassium ions through the membrane. It is necessary to maintain neuronal excitability. The malfunction of this enzyme has been associated with neuronal hyperexcitability. The pilocarpine-induced status epilepticus in developing rats leads to neuronal hyperexcitability and brain damage. We examined the activity of the Na(+)/K(+)ATPase enzyme in hippocampus of rats submitted to 1 episode of status epilepticus on postnatal day 9 and to 3 episodes of pilocarpine-induced status epilepticus on postnatal days 7, 8 and 9. Our findings showed that one status epilepticus episode does not modify the Na(+)/K(+)ATPase activity in hippocampus of rats studied 7 or 30 days later (at P16 or P39). However, an increase in the Na(+)/K(+)ATPase activity was detected in hippocampus of rats submitted to three consecutive status epilepticus during the development studied 7 (+142%) and 30 (+400%) days following the injections. In addition, a significant reduction in the Na(+)/K(+)ATPase activity was observed in control rats at P39 compared to P16. Our data suggest that multiple pilocarpine-induced status epilepticus in developing rats induce long-lasting increase in the Na(+)/K(+)ATPase activity in the hippocampus, reflecting hyperexcitability.
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PMID:The Na+/K+ATPase activity is increased in the hippocampus after multiple status epilepticus induced by pilocarpine in developing rats. 1727 Jan 50

Innate immunity mediated by microglia appears to play a crucial role in initiating and propagating seizure-induced inflammatory responses. To address the role of activated microglia in the pathogenesis of childhood epilepsy, we first examined the time course of microglia activation following kainic acid-induced status epilepticus (KA-SE) in Cx3cr1(GFP/+) transgenic mice whose microglia are fluorescently labeled. We then determined whether this seizure-induced microglia activation primes the central immune response to overreact and to increase the susceptibility to a second seizure later in life. We used an inhibitor of microglia activation, minocycline, to block the seizure-induced inflammation to determine whether innate immunity plays a causal role in mediating the long-term epileptogenic effects of early-life seizure. First status epilepticus was induced at postnatal day (P) 25 and a second status at P39. KA-SE at P25 caused nearly a two-fold increase in microglia activation within 24h. Significant seizure-induced activation persisted for 7 days and returned to baseline by 14 days. P39 animals with prior exposure to KA-SE not only responded with greater microglial activation in response to "second hit" of KA, but shorter latency to express seizures. Inhibition of seizure-induced inflammation by 7 day minocycline post-treatment abrogated both the exaggerated microglia activation and the increased susceptibility to the second seizure later in life. The priming effect of early-life seizures is accompanied by modified and rapidly reactivated microglia. Our results suggest that anti-inflammatory therapy after SE may be useful to block the epileptogenic process and mitigate the long-term damaging effects of early-life seizures.
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PMID:Minocycline attenuates microglia activation and blocks the long-term epileptogenic effects of early-life seizures. 2236 82