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

The time course of changes in behaviour, seizure response and cerebral monoamine and gamma-aminobutyric acid (GABA) metabolism has been studied in relation to the anticonvulsant actions of di-n-propylacetic acid (DPA) and ethanolamine-O-sulphate (EOS) on sound-induced seizures in DBA/2 mice. Changes in cerebral monoamine metabolism after EOS (75 or 150 mug, intracerebroventricularly) were not related to its anticonvulsant action. The primary effect was GABA-transaminase inhibition (by 50-70%) leading to a 2-4 fold increase in cerebral GABA concentration. Increases in brain GABA concentration (maximally 36%), 5-hydroxyindoleacetic acid (5HIAA, maximally 134%) and homovanillic acid (HVA, maximally 183%) were seen after DPA (400-600 mg/kg, i.p.). The time course of the increases in HVA and 5HIAA did not correlate with the anticonvulsant effect. Elimination of these increases by the use of inhibitors of monoamine synthesis (alpha-methyl-p-tyrosine and p-chlorophenyl-alanine) did not alter the anticonvulsant effect of DPA. Experiments using probenecid suggested that the increases in 5HIAA and HVA after DPA result from inhibition of their active transport out of the brain.
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PMID:Monoamine and GABA metabolism and the anticonvulsant action of di-n-propylacetate and ethanolamine-O-sulphate. 13 17

Spinal cord transection affords protection from audiogenic seizures (anterior to paralysis) in 21 day-old DBA/2J mice. To test the possibility that altered brain levels of NE or 5-HT are involved in mediating this effect, whole brain levels of these amines were assayed in cordotomized and control DBA/2J mice, aged 21 days. The assay revealed no significant differences between cordotomized and control mice. Therefore, cordotomy protects mice from seizures by mechanisms other than altering brain levels of NE or 5-HT.
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PMID:Changes in brain levels of NE and 5-HT are not responsible for attenuation of audiogenic seizures by spinal cordotomy. 28 80

Serum thyroxine levels peak earlier and are significantly higher in audiogenic seizure-susceptible DBA/2J mice than in seizure-resistant C57BL/6J mice during early postnatal life. The seizure susceptibility of DBA/2J mice is suppressed by administration of an antithyroid drug or by radiothyroidectomy, while the seizure susceptibility of C57BL/6J mice is enhanced by treatment with excess thyroxine.
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PMID:Thyroid hormone influence on the susceptibility of mice to audiogenic seizures. 45 24

Compounds blocking the uptake of GABA into neurons or glia have been injected intracerebroventricularly (icv) or intraperitoneally (ip) in DBA/2 mice, age 21-28 days. Protection against audiogenic seizures was seen 30 min after the icv injection of (+)-2,4-diaminobutyric acid (0.5-2.0 mumoles), (+/-)-nipecotic acid (1.6-3.2 mumoles), (+)-ethyl nipecotate (0.4-0.8 mumoles), (-)-piperazic acid (4 mumoles) and putrescine (2 mumoles) or the ip injection of (+)-2,4-diaminobutyric acid (4-8 mmoles/kg and (+)-ethyl nipecotate (0.24-0.32 mmoles/kg). Of these ethyl nipecotate and nipecotic acid were the most effective anticonvulsants icv, but nipecotic acid was ineffective ip. Limb myoclonus and other epileptic manifestations (rearing, wild running, tonic clonic seizures) occurred in the absence of auditory stimulation after (+)-2,4-diaminobutyric acid (0.5-2.0 mumoles), (+/-)-cis-3-aminocyclohexane carboxylic acid (3.2-6.4 mumoles) and putrescine (2 mumoles). beta-Alanine (2-4 mumoles, icv) depressed respiration but did not protect against audiogenic seizures or induce myoclonus.
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PMID:Convulsant and anticonvulsant actions in DBA/2 mice of compounds blocking the reuptake of GABA. 51 Apr 1

Parent C57BL/10Bg and DBA/1Bg inbred mice were fed 10% ethanol in their drinking solution during mating and pregnancy and/or early post parturition period. The susceptibility to audiogenic seizures and the open field behavior of their offspring were tested at age 29--33 days. Our previous experiments have indicated that continuous exposure to ethanol during pre- and neonatal periods enhanced the susceptibility to audiogenic seizures in both strains and decreased open field activity only in the strain C57. The present study, while confirming previous findings, assessed the relative contribution of the prenatal and the neonatal administration of ethanol to the behavioral changes. Among C57 mice, the neonatal period was most important for the induction of changes in seizures, but prenatal exposure which alone had no effect, enhanced the outcome of neonatal administration. Among DBA mice either period induced seizures, but the contribution of the neonatal period was the most significant. Early ethanol administration affected open field behavior only in C57 mice. There was an additive interaction between the two periods (latency), no effect by any period alone but together they produced a full effect (ambulation), or that either period alone was sufficent to produce a full effect (defecation).
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PMID:The relative contribution of pre- and neonatal ethanol administration to changes in mice behavior. 52 78

We have investigated the relationship between catecholamine turnover and susceptibility to audiogenic seizures (AGS) in the developing DBA/2J mouse. Turnover of dopamine and norepinephrine was determined after administration of alphamethylparatyrosine at 3 weeks of age when nearly all mice (94%) exhibited AGS, at 6 weeks when only 30% were susceptible, and at 12 weeks when none developed seizures. Turnover of brain dopamine increased progressively from 236 ng/g/hr at 3 weeks to 389 ng/g/hr by 12 weeks of age. Norepinephrine turnover increased significantly between 3 and 6 weeks of age, then remained stable thereafter. Turnover times for each catecholamine did not change appreciably with maturation. Our results support the notion that susceptibility to AGS may be mediated in part by brain catecholaminergic mechanisms.
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PMID:Ontogeny of brain catecholamine turnover and susceptibility to audiogenic seizures in DBA/2J mice. 65 4

In baboons, Papio papio, spontaneously showing photosensitive epilepsy, myoclonic responses to intermittent photic stimulation were reduced or abolished for up to four hours by (+/-)-N-n-propylnorapomorphine (NPA) 0.05-0.2 mg/kg body weight, given i.v. In animals pretreated with allyglycine, 200 mg/kg, a transient abolition of myoclonic responses followed NPA, 0.2 mg/kg. In DBA/2 mice, seizures following auditory stimulation were attenuated or abolished by NPA 0.025-0.1 mg/kg given intraperitoneally (ED50 for abolition of clonic phase = 0.032 mg/kg). The ED50 for pentylenetetrazol seizures in MF 1 mice was not altered by NPA 0.25 mg/kg.
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PMID:Inhibition of reflex epilepsy by (+/-)-N-n-propylnorapomorphine. 82 45

Metopyrone, an inhibitor of glucocorticoid synthesis, blocks the development of susceptibility to audiogenic seizures in C57BL/6Bg mice after either acoustic priming at 19 days of age or ethanol withdrawal at 70-80 days of age, whereas it has no effect on the development of genetic susceptibility in DBA/1Bg mice. This suggests that there may be similar developmental mechanisms for effects of acoustic priming and ethanol withdrawal on audiogenic seizure risk, which may be different from that for the genetic susceptibility of DBA/1Bg mice.
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PMID:Glucocorticoids and development of audiogenic seizure susceptibility in DBA/1Bg mice. 91 3

gamma-Acetylenic GABA and gamma-vinyl GABA, two catalytic irreversible inhibitors of GABA-transaminase, produce marked and sustained elevations in mouse brain GABA concentrations and protect DBA/2 mice against audiogenically induced seizures in a similar dose and time-dependent manner. The acetylenic analog also inhibits GAD activity while the vinyl compound has minimal activity against this enzyme. The increase in brain GABA concentrations induced by these compounds correlates well with attenuation of audiogenic seizure intensity (r = 0.991 and 0.962 for gamma-acetylenic and gamma-vinyl GABA respectively) and with degree of seizure protection (r = 0.974 and 0.834). Seizure intensity is reduced by 50% when brain GABA is increased to 265% and 264% of control values by the two inhibitors and seizure incidence is halved at 322% and 324%. Thus, audiogenic seizure protection in genetically susceptible mice is apparently a function of whole brain GABA concentrations.
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PMID:Audiogenic seizure protection by elevated brain GABA concentration in mice: effects of gamma-acetylenic gaba and gamma-vinyl GABA, two irreversible GABA-T inhibitors. 92 42

Susceptibility to audiogenic seizures can be induced in some strains of resistant mice by exposure to an initial auditory stimulus (acoustic priming). Aminooxyacetic acid, hydrazine, glutamic acid, gamma-aminobutyric acid (GABA), cycloheximide, and metyrapone antagonize the acoustic priming of audiogenic seizure susceptibility in C57BL/6Bg mice, whereas only metyrapone attenuates that of DBA/1Bg-asr mice. The strain difference in the effect of AOAA and cycloheximide is correlated with a small, transient fall in level of brain GABA in C57BL/6Bg but not DBA41Bg-asr mice. These findings support our hypothesis that there are at least two neural mechanisms of acoustic priming, each with its own genetic basis and that corticosteroids are required by both mechanisms for the development of primed seizures.
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PMID:Pharmacogenetic differences in audiogenic seizure priming of C57BL/6Bg and DBA/1Bg-asr mice. 92 78


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