Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The audiogenic seizure-inducing drug H13/04 was found to elicit opposing effects on the in vivo accumulation of 5-HTP (5-hydroxytryptophan) and DOPA (3,4-dihydroxyphenylalanine) in the brain following inhibition of L-amino acid decarboxylase. In strains of mice that normally do not exhibit audiogenic seizures, H13/04 retarded the accumulation of 5-HTP in the telencephalon, diencephalon and brainstem and enhanced the accumulation DOPA in the diencephalon and brainstem. The duration of the biochemical action of H13/04-correlated with the duration of the behavioral effect. When H13/04 is administered to strains of mice with a genetically-determined susceptibility to audiogenic seizures, but at an age when they are developing resistance to seizures, H13/04 does not alter the incidence of sound-induced seizures. The effect on the accumulation of 5-HTP and DOPA was similar to that noted in the genetically-resistant strain; a retardation of the accumulation of 5-HTP in the telencephalon and brainstem and an enhancement of DOPA accumulation in the brainstem. Since the rate of accumulation of 5-HTP and DOPA is a measure of the in vivo rates of tryptophan and tyrosine hydroxylase, respectively, the results may reflect changes in neural activity with consequent effects on the synthesizing enzymes. These results emphasize the usefulness of the drug in analyzing central mechanisms underlying audiogenic seizure activity and in studying functional properties and interactions of the central catechol-and indoleamine systems.
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PMID:Central action of a catechol-amide seizure-inducing agent: opposing effect on tyrosine and tryptophan hydroxylase activity in vivo. 0 34

5-Hydroxytryptophan (5-HTP) reduced the intensity of both audiogenic and pentylenetrazol seizures. p-Chlorophenylalanine reduced audiogenic seizure (AGS) susceptibility but failed to change the pentylenetetrazol seizure (PTS). Drugs blocking brain serotonin (5-HT) receptors suppressed AGS but caused no clear effects upon PTS. Pentylenetetraziol-induced shock increased brain 5-hydroxyindoleacetic acid (5hiaa) concentrations and decreased 5-HT levels. Single audiogenic shock decreased the acumulation of 5-HT and 5-HIAA in the brains of mice pretreated with 5-HTP. On the other hand PTS increased the accumulation of 5-HT and 5-HIAA in the brains of mice pretreated with 5-HTP. It is suggested that AGS decrease brain 5-HT turnover whilst PTS cause an opposite effect.
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PMID:Brain serotonin and epileptic seizures in mice: a pharmacological and biochemical study. 14 40

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

Intravenous infusions were used to produce physical dependence upon ethanol in rats. The procedure proved to be safe, rapid, and reliable. Ethanol (30% v/v) was administered over a 7-day period. The mean daily dose ranged from 10--14 g/kg/day. Control rats were exposed to a comparable procedure except that saline, rather than ethanol, was infused. All ethanol treated rats that survived the intoxication period (n = 11) showed signs of physical dependence (moderate to severe, n = 8; mild, n = 3) following ethanol withdrawal. Saline treated rats (n = 8) did not show any of these symptoms. The most reliable ethanol withdrawal signs observed were: spontaneous seizure (n = 7), audiogenic seizure (n = 7), tremors (n = 6), tail stiffening (n = 10) and body rigidity (n = 9). These symptoms were analyzed in terms of their hour of onset and hour of maximum intensity following ethanol withdrawal. Application of the intravenous method for the study of ethanol self-administration is discussed.
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PMID:Induction of physical dependence upon ethanol in rats using intravenous infusion. 56 3

Glucose and insulin injections both decrease seizure susceptibility in C57BL/6J mice subjected to audiogenic priming at 16 days of age and tested at 21 days of age. These data support an hypothesis of defect in immediately available energy reserves in brains of audiogenic seizure prone mice.
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PMID:Time course of protection from audiogenic seizures by glucose and insulin in audiogenically primed C57BL/6J mice. 67 68

A comparison of the anticonvulsant and neurotoxic effects of cannabidiol (CBD), delta 9tetrahydrocannabinol, cannabinol and antiepileptic drugs (phenytoin, phenobarbital, carbamazepine, chlordiazepoxide, clonazepam, ethosuximide and trimethadione) was made in rats. Median effective potencies (ED 50 values) for maximal electroshock, audiogenic seizures and TD50 values for a rotor rod neurotoxicity test were calculated. Additionally, the interactive effects of CBD and the antiepileptic drugs against maximal electroshock and audiogenic seizures were studied. Each drug was given orally at peak effect time. CBD was an effective and relatively potent anticonvulsant in both maximal electroshock and audiogenic seizure tests. The anticonvulsant potency of phenytoin was significantly increased when combined with phenobarbital, CBD and phenobarbital plus CBD. Additionally, CBD reliably reduced the anticonvulsant potencies of chlordiazepoxide, clonazepam, trimethadione and ethosuximide. These data indicate that CBD is an effective anticonvulsant with a specificity more comparable to drugs clinically effective in major than minor seizures. Furthermore, it appears that CBD enhances the anticonvulsant effects of the former and reduces the effects of the latter types of antiepileptic drugs.
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PMID:Cannabidiol--antiepileptic drug comparisons and interactions in experimentally induced seizures in rats. 85 Jan 45

gamma-Acetylenic gamma-aminobutyric acid (gamma-acetylenic GABA) produces several-fold sustained elevations of brain GABA concentrations when administered intraperitoneally to mice. It protects mice against seizures induced by audiogenic stimuli, electroshock, thiosemicarbazide, isoniazid and strychnine. The duration and degree of audiogenic seizure protection appears to correlate with elevations in whole brain GABA levels. gamma-Acetylenic GABA does not protect against seizures induced by pentylenetetrazol or picrotoxin even at doses that increase brain GABA concentrations approximately 6-fold. This differential antiseizure activity suggests that the GABA system may play a role in some, but not all experimentally produced seizures.
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PMID:Antiseizure activity of gamma-acetylenic gamma-aminobutyric acid: a catalytic irreversible inhibitor of gamma-aminobutyric acid transaminase. 86 98

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

A relatively stereotyped seizure reaction can be triggered by the "offset" of an intense bell sound in C57BL/6J mice. Susceptibility to this offset-induced audiogenic seizure was found to depend upon the age of the animals tested (higher in older mice) and the duration of the noise exposure (more effective with longer exposure).
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PMID:Offset-induced audiogenic seizures. 92 11


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