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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of local application of taurine and isethionic acid on the propagation of the epileptic activity to the mirror area in cats have been studied. Cortical and amygdaloid acute foci were induced by local administration of conjugated estrogens. Taurine proved to be effective in reducing and sometimes in abolishing the appearance of the epileptic propagated elements in the mirror area. When this agent was applied 30 minutes before the induction of the primary focus, the single spike transmission was reduced or prevented; however, the transmission of a seizure was not blocked. No changes in the transmitted phenomena were observed when isethionic acid was administered with the same technique as that used for taurine. The present study stresses the clear antiepileptic activity of taurine in this experimental model, ruling out the possibility of an unspecific interaction with the epileptogenic agents. Moreover, it is suggested that the deamination of taurine is not important for its antiepileptic action.
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PMID:Cortical and subcortical projected foci in cats: inhibitory action of taurine. 17 98

Taurine was effective in reducing the hypnotic effect of ethanol but did not antagonize the effect of ethanol on seizure susceptibility, body temperature, or brain 5-HIAA concentration.
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PMID:Effect of taurine on some pharmacological properties of ethanol. 73 33

The anticonvulsive action of taurine, was tested in 9 therapy in 9 therapy-resistant patients with a high incidence of seizures. Taurine was given orally (1.5-7.5 g daily) over a period of 4 to 16 weeks and, despite the high dosage, no appreciable side effects were observed. During this time seizures disappeared temporarily for about two weeks in 5 out of 9 cases. In one case the seizure frequency was transiently reduced by approximately 25%, whilst in the remaining 3 cases no effect of taurine on seizure frequency was observed. The reason for the rapid disappearance of the anticonvulsive action of taurine is not known.
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PMID:[Orally-administered taurine in therapy-resistant epilepsy (author's transl)]. 83 13

Intra-amygdaloid injections of gamma-glutamyltaurine, a recently identified brain dipeptide, strongly suppressed seizures in amygdala-kindled rats stimulated with intensities 10 or 50 microA above the generalized seizure triggering threshold (mean 82 microA). The suppressive effect persisted as long as 3 days. Taurine had relatively weak suppressive effects. Thus gamma-glutamyltaurine seems much more potent than taurine in the suppression of epileptic seizures when injected directly into the kindling site.
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PMID:Gamma-glutamyltaurine has potent and long-lasting antiepileptic action as demonstrated by intra-amygdaloid injection in amygdala-kindled rats. 145 Sep 62

The susceptibility of rats made deficient of taurine by treatment with guanidinoethane sulfonate (GES), to seizures induced by 4-aminopyridine was examined. Guanidinoethane sulfonate, at a concentration of 1% was administered to pregnant rats, in the drinking water 2-3 days prior to delivery and the treatment was continued during nursing. Pups were weaned to the same treatment until 6 weeks of age. This treatment decreased levels of taurine in the cerebral cortex by 70%. 4-Aminopyridine was injected intraperitoneally at doses ranging from 4-7 mg/kg. Taurine-deficient rats showed a greater susceptibility to seizures, as demonstrated by a lowered latency for clonic seizures, an increased incidence of tonic seizures and a higher postseizure mortality. These results suggest an involvement of endogenous taurine in nervous excitability.
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PMID:Higher susceptibility of taurine-deficient rats to seizures induced by 4-aminopyridine. 283 May 54

Extracellular amino acid levels in the rat piriform cortex, an area highly susceptible to seizure-induced neuropathology, were determined by means of intracranial microdialysis. Seizures were induced by systemic administration of either soman (O-1,2,2-trimethylpropyl methylphosphonofluoridate), a potent inhibitor of acetylcholinesterase, or the excitotoxin kainic acid. Extracellular glutamate levels increased in animals with seizures shortly after administration of either convulsant, but this change was statistically significant only in the case of soman-treated animals. Extracellular taurine levels increased markedly, reaching two- and fourfold baseline levels during the second hour of soman- and kainic acid-induced seizures, respectively. Taurine levels did not increase in the subpopulation of soman-treated animals without seizures, a finding indicating that elevation of extracellular taurine level is seizure related. Thus, we propose that taurine efflux may be a physiological cellular response to neuronal changes produced by excitotoxic chemicals, either directly or as a consequence of seizures.
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PMID:Changes in extracellular amino acids during soman- and kainic acid-induced seizures. 359 90

The part played by taurine in epileptogenesis is still controversial. A cortical deficit of the amino acid has been confirmed only in certain types of human and animal epilepsy, and the effects of an artificial change of taurine cortical concentration are inconclusive. An increase is associated with a reduced susceptibility to epileptogenic agents but not with the prevention of epilepsy, while a decrease may precipitate seizure activity in genetically susceptible rats but does not bring about spontaneous epileptic activity in normal animals. The role of taurine in synaptic transmission is uncertain (specific inhibitory neurotransmitter, indirect modulator of membrane excitability), and its antiepileptic action, confirmed in several models of experimental epilepsy and in short-term clinical studies, does not seem to possess major clinical relevance since trials with a longer follow-up gave unsatisfactory results. Taurine's limited diffusibility across the blood-brain barrier may be the main factor restricting the antiepileptic effect of this compound.
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PMID:The current status of taurine in epilepsy. 634 65

The decreased microsomal Ca++Mg++ATPase activity and lowered level of Ca++ binding by the brain cortex microsomes in seizure prone rats as compared with normal animals have been revealed. Taurine increases these parameters in experiments in vitro. Injection of taurine into the penicillin-provoked epileptogenic focus prevents the seizure reaction in rabbits. This effect is not observed after injection of taurine together with EGTA. The data obtained demonstrate the important role of calcium ions in the anticonvulsant action of taurine.
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PMID:[Role of calcium ions in the evolution of the anticonvulsant effect of taurine]. 644 35

Taurine was administered orally to 25 intractable epileptic children, ranging in age from 4 months to 12 years. All patients had been suffered from frequent seizures daily in spite of vigorous anticonvulsant medication. Daily taurine doses ranged from 0.05 to 0.3 g/kg. Twelve patients received probenecid additionally in doses ranging from 0.5 to 1.0 g/day. Complete control of seizures was achieved in a case of Lennox syndrome, over 50% decrease of seizure frequency in 1 case, less than 50% decrease in 4 cases, and no effects in 18 cases. The effects of taurine often manifest only temporarily. Electroencephalographic abnormalities did not improve by taurine in 21 cases examined except 1 in which EEG markedly ameliorated along with clinical seizure control. In 6 patients, the concentration of taurine in CSF and serum did not change but urinary excretion increased. Four patients exhibited side effects of drowsiness and ataxia.
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PMID:Therapeutic trial by taurine for intractable childhood epilepsies. 703 91

Pretreatment of rats with homotaurine (3 aminopropanesulfonic acid; 3APS), a synthetic gamma-aminobutyric acid (GABA) analog, protected from the convulsant and cytotoxic action of systemically injected kainic acid (KA). Wet dog shaking (WDS) behavior was significantly reduced. Taurine, an inhibitory non-GABA-mimetic amino acid, and muscimol (another direct GABA-agonist) reduced the number of seizures and lesions in the brain but were less effective than homotaurine. Progabide (a GABA-agonist) did not modify kainic acid effects. The neurotoxicity of kainic acid could have been due to repetitive convulsive activity. Activation of GABA-mediated inhibition is an effective, but not the determinant means of preventing KA-induced abnormalities.
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PMID:Homotaurine (3 aminopropanesulfonic acid; 3APS) protects from the convulsant and cytotoxic effect of systemically administered kainic acid. 719 33


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