anthranilic acid/seizures

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Evidence that kynurenine pathway metabolites mediate hyperbaric oxygen-induced convulsions.

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Metabolism of tryptophan (TRP) through the kynurenine (KYN) pathway in brain, liver, and kidney produces intermediates including the neuroactive agonist quinolinic acid (QA) and the antagonists kynurenic acid (KA) and anthranilic acid (AA) for N-methyl D-aspartate (NMDA) receptors in the central

Antagonism of kynurenine-induced seizures by picolinic, kynurenic and xanthurenic acids.

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Picolinic, kynurenic, xanthurenic and anthranilic acids are metabolites of L-kynurenine which, when administered intraperitoneally (i.p.) antagonized (in descending order of potency) the seizures induced by intracerebroventricular (i.c.v.) injections of l-kynurenine sulfate in SHR and C57BL/6 mice.

Synthesis of some new thioxoquinazolinone derivatives and a study on their anticonvulsant and antimicrobial activities.

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OBJECTIVE A series of ten novel derivatives of 3-substituted-2-thioxoquinazolin-4(3H)-ones have been synthesized from anthranilic acid via Mannich reaction with various secondary amines in presence of formaldehyde in ice cold condition. METHODS The structure of these compounds have been elucidated

Synthesis of previously inaccessible quinazolines and 1,4-benzodiazepines as potential anticonvulsants.

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A series of 4,6,7,8- tetrasubstituted 3,4- dihydroquinazolines , quinazolines, quinazolin -2-ones, 1,2,3,4- tetrahydroquinazolin -2-ones, and 5,7,8,9- tetrasubstituted 1,4-benzodiazepines have been synthesized by utilizing the Diels -Alder reaction between furan o-amino nitriles and various alkyl or

Comparison of the neurochemical and behavioral effects resulting from the inhibition of kynurenine hydroxylase and/or kynureninase.

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Several kynurenine analogues were synthesized and tested as inhibitors of the enzymes kynurenine hydroxylase and/or kynureninase with the aim of identifying new compounds able to inhibit the synthesis of quinolinic acid (an endogenous excitotoxin) and to increase that of kynurenic acid, an

[Enhancement of the convulsant action of strychnine following administration of kynurenines into the cerebral ventricles of frogs].

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In frogs (Rana temporaria) injection of L-kynurenine, quinolinic, nicotinic and picolinic acids (10 microgram) into brain ventricles potentiated the stimulant ad convulsant effects of a subthreshold dose of strychnine. Xanthurenic and anthranilic acids were ineffective. At a dose of 100 micrograms

Effect of kynurenine and quinolinic acid on the action of convulsants in mice.

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Intraventricular injection of DL-kynurenine and L-kynurenine sulfate (40 microgram) into conscious mice potentiated convulsions and lethality produced by strychnine (1 mg/kg) and not by thiosemicarbazide nor pentylenetetrazol. Another metabolite of tryptophan with convulsive effect, quinolinic acid,

The effects of vagus nerve stimulation on tryptophan metabolites in children with intractable epilepsy.

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BACKGROUND The mechanism of action of vagus nerve stimulation (VNS) in intractable epilepsy is not entirely clarified. It is believed that VNS causes alterations in cytokines, which can lead to rebalancing the release of neurotoxic and neuroprotective tryptophan metabolites. We aimed to evaluate VNS

Stimulant and convulsive effects of kynurenines injected into brain ventricles in mice.

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Each of six kynurenines tested (DL-kynurenine, quinolinic, 3-hydroxy-anthranilic, xanthurenic, picolinic, and nicotinic acids) injected into brain ventricles in mice in doses of 25--60 mcg produced motor excitement and/or clonic convulsions. Anthranilic acid did not produce these effects. The

Tryptophan metabolism and brain function: focus on kynurenine and other indole metabolites.

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The synthesis of NAD (or NADP) from tryptophan involves a series of enzymes and the formation of a number of intermediates which are collectively called 'kynurenines.' In the late 1970s and early 1980s, it became clear that intraventricular administration of several 'kynurenines' could cause

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