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 the inhibition of carbonic anhydrase on the manifestation of tonic-clonic seizures were investigated in freely-moving rats. 4-Aminopyridine, a specific blocker of the neuronal K+ channels was used to produce generalized convulsions. After pretreatment of adult male rats with 20 or 40 mg/kg acetazolamide, 3, 5, 7 or 9 mg/kg 4-aminopyridine was injected intraperitoneally and the latencies of the symptoms were measured. Pharmacological inhibition of brain carbonic anhydrase significantly increased the latency of onset of seizures. Bolus administration of acetazolamide decreased the incidence of generalized convulsions and protected against status epilepticus. Chronic acetazolamide treatment for 2 days affected only the generalized convulsions. The results suggested that alterations of the extracellular and intracellular pH by acetazolamide decreased the efficacy of synaptic transmission in several areas of the brain. The possible effects of the HCO3- ions on the sensitivity of synaptic and nonsynaptic neuronal receptors are discussed.
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PMID:Pharmacological inhibition of brain carbonic anhydrase protects against 4-aminopyridine seizures. 788 80

Limited data exist on overdose with new antiepileptic drugs. We reviewed the medical records of two patients who took a topiramate overdose as a suicide attempt. We recorded their medical and seizure histories, concomitant antiepileptic medications, neurologic examination, and laboratory findings at the time of presentation following the overdose. We also recorded their progress and the evolution of laboratory abnormalities. Both patients progressed to coma and had generalized convulsive status epilepticus, requiring intubation and treatment with benzodiazepines. Both patients recovered within 2 days but had a non-anion-gap metabolic acidosis that persisted for 5-6 days. Physicians should carefully monitor patients treated with topiramate who develop signs of clinical depression. The non-anion-gap metabolic acidosis observed may be due to inhibition of renal cortical carbonic anhydrase.
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PMID:Topiramate Overdose: Clinical and Laboratory Features. 1260 21

Experimental and theoretical evidence indicates that GABAergic neurotransmission is fundamental for the synchronization of neuronal activity. In particular, the role of GABA in epileptiform activity has received increased attention due to, among others, the fact that the GABA-mediated potentials can be depolarizing, and hence excitatory, in some circumstances. Evidence is presented here that bicarbonate efflux via GABAA receptors in interneurons and pyramidal cells of the CA1 hippocampal area contribute to depolarizing GABAA-mediated potentials in an in vitro nonpharmacological seizure-like model of status epilepticus. Seizure-like and interictal activity was evoked in rat horizontal hippocampal slices using a superfusing solution with low magnesium concentration (0.5-0.9 mm). Whole-cell recordings from stratum oriens-alveus interneurons and CA1 pyramidal cells revealed that, during epileptiform activity, some GABAA-mediated potentials were depolarizing, and were suppressed by the carbonic anhydrase inhibitor ethoxyzolamide as well as by the GABAA-receptor antagonist bicuculline. These observations indicate that the depolarizing potentials observed during epileptiform activity reflect both glutamatergic and GABAA-receptor-mediated activity, and adds further support for the important role of GABAergic interneurons in promoting long-range synchronization.
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PMID:Bicarbonate-dependent depolarizing potentials in pyramidal cells and interneurons during epileptiform activity. 1295 33