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Protective action of nicotinic acid benzylamide in a variety of chemically-induced seizures in mice.

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OBJECTIVE The study aims to assess the anticonvulsant effects offered by benzylamide nicotinic acid (Nic-BZA) in many animal models of chemically-induced seizures (i.e., pentylenetetrazole [PTZ], pilocarpine [PILO], bicuculline [BIC], α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid [AMPA],

[Tryptophan metabolism "via" nicotinic acid in children with febrile convulsions].

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In silico validation and structure activity relationship study of a series of pyridine-3-carbohydrazide derivatives as potential anticonvulsants in generalized and partial seizures.

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A series of twelve compounds (Compounds RNH1-RNH12) of acid hydrazones of pyridine-3-carbohydrazide or nicotinic acid hydrazide was synthesized and evaluated for anticonvulsant activity by MES, scPTZ, minimal clonic seizure and corneal kindling seizure test. Neurotoxicity was also determined for

Anticonvulsant and acute neurotoxic characteristics of nicotinic acid benzylamide: a preclinical study.

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The aim of this study was to evaluate time-course and dose-response relationships of nicotinic acid benzylamide (Nic-BZA) with regard to its anticonvulsant activity in the maximal electroshock (MES)-induced seizures and acute neurotoxic effects in terms of motor coordination impairment in the

Assessment of the anticonvulsant potency of various benzylamide derivatives in the mouse maximal electroshock-induced seizure threshold model.

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OBJECTIVE The aim of this study was to assess the anticonvulsant potency of 6 various benzylamide derivatives [i.e., nicotinic acid benzylamide (Nic-BZA), picolinic acid 2-fluoro-benzylamide (2F-Pic-BZA), picolinic acid benzylamide (Pic-BZA), (RS)-methyl-alanine-benzylamide (Me-Ala-BZA),

Antagonism of seizures induced by the administration of the endogenous convulsant quinolinic acid into rat brain ventricles.

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The effect of pretreatment with drugs on generalized clonic-tonic seizures induced by intracerebroventricular (i.c.v.) administration of the endogenous convulsant quinolinic acid (QUIN, 50 micrograms) was studies in rats. Of the inhibitory amino acids tested, only 1-glycine (50 and 100 micrograms,

In vivo brain dialysis of amino acids and simultaneous EEG measurements following intrahippocampal quinolinic acid injection: evidence for a dissociation between neurochemical changes and seizures.

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The extracellular content of taurine, glutamate, glutamine, and glycine was measured by the novel method of brain dialysis in the acute phases following an intrahippocampal injection of the excitotoxic convulsant brain metabolite quinolinic acid (QUIN). Using bilaterally implanted depth electrodes

Nicotinamide, inosine and hypoxanthine, putative endogenous ligands of the benzodiazepine receptor, opposite to diazepam are much more effective against kynurenine-induced seizures than against pentylenetetrazol-induced seizures.

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Nicotinamide (NAM, 1000 mg/kg), inosine (INS, 1000 mg/kg), hypoxanthine (HXT, 500 mg/kg), putative endogenous ligands of the benzodiazepine receptor, and nicotinic acid (NA, 500 mg/kg) diminished DL-kynurenine-(DL-K, 50 micrograms ICV) induced seizures in C57BL/6 adult male mice and only prolonged

Vitamins in psychiatry. Do they have a role?

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Deficiencies of specific vitamins produce consistent symptoms of psychiatric disorder. Thiamine deficiency, which is common in alcoholism, can produce confusion and psychotic symptoms, in addition to neurological signs. Vitamin B12 and folate deficiency may contribute symptoms of disorientation,

[Decrease in the activity of cerebral gamma-aminobutyric acid metabolism enzymes under the influence of kynurenines possessing convulsive activity].

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Content of gamma-aminobutyric acid (GABA) was unaltered in mouse brain and cerebellum after administration of D,L-kynurenine (50 mcg), quinolinic acid (5 mcg) and nicotinic acid (50 mcg) into brain ventricles. At the same time, after administration of kinurenine, quinolinic acid and nicotinic acid

[Vitamins in metabolic diseases].

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Several vitamins have been demonstrated to interfere with the pathogenesis of some metabolic diseases, mainly by three different mechanisms: 1) vitamin malabsorption, 2) errors in vitamin metabolism, 3) vitamin dependent syndromes. The latter is due to a deficiency of the apoenzyme whose coenzyme is

[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

Alcoholic Pellagra as a Cause of Altered Mental Status in the Emergency Department.

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BACKGROUND Pellagra, which is caused by a deficiency of niacin and tryptophan, the precursor of niacin, is a rare disease in developed countries where alcoholism is a major risk factor due to malnutrition and lack of B vitamins. Although pellagra involves treatable dementia and psychosis, it is

Studies on the potential neurotoxic and convulsant effects of increased blood levels of quinolinic acid in rats with altered blood-brain barrier permeability.

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Intravenous injection of 450 mg/kg quinolinic acid (Quin), an endogenous kynurenine metabolite with excitotoxic properties, induced only minor electroencephalographic (EEG) modifications and no neurotoxicity in rats with a mature blood-brain barrier (BBB). BBB permeability was altered in rats by

[Stimulatory effects of intraventricular administration of kynurenines, amino acids, and convulsants: differences between rats and mice].

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Quinolinic acid appeared to be the only kynurenine metabolite among tested (L- and DL-kynurenine sulfate, kynurenic and nicotinic acids, nicotinamide) which induced locomotor excitation and clonic seizures in rats whereas all of them exerted convulsant action in mice. Excitatory 1-glutamic and

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