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

Intraperitoneal injection of nicotinamide to rats inhibits epileptic activity induced by penicillin application in the animals' brain cortex. It has been found in experimental primary-generalized epileptic activity induced by bemegride that preliminary injection of nicotinamide increased the latency of the emergence of the first epileptic seizures. Addition of nicotinamide to synaptosomal suspension inhibited accumulation in it of the products of lipid peroxidation. Relationship between antioxidant properties of nicotinamide and its antiepileptic activity is discussed.
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PMID:[Effect of nicotinamide on focal and generalized epileptic activity in the cerebral cortex]. 621 72

Effects of different doses of nicotinamide, pantogam, pnenazepam, and their combined actions on generalized seizures induced by pentylenetetrazole (60-100 mg/kg) were studied in acute experiments on mice. It was shown that pantogam (500 mg/kg) doubled the latent period of seizures, considerably attenuated the intensity of attacks and lethality, whereas given in a dose of 1000 mg/kg it completely prevented the animals' death. Nicotinamide (250-500 mg/kg) increased the latent period of seizures without affecting the intensity of seizures or lethality. Nicotinamide (1000 mg/kg) prevented the development of clonico-tonic attacks and lethality. The antiseizure effects of nicotinamide depended on the time of its injection. Phenazepam (1.4 mg/kg) abolished seizures and in a dose of 0.1-0.7 mg/kg protected the animals from death and considerably relieved seizure manifestations. During combined injections of these compounds, the antiseizure effect was more pronounced and could be attained by decreasing the drug doses.
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PMID:[Effect of pantogam, nicotinamide, and phenazepam on seizure activity]. 621 28

In adult male albino BALB/c mice inosine (INS, 100 and 200 micrograms, intraventricularly) prolonged the latency of pentylenetetrazol (PTZ) seizures while nicotinamide (NAM) exerted an opposite effect. In adult male C57BL/6 mice INS decreased lethality after PTZ while NAM increased it. In adult male albino SHR (bred from Swiss) and in adult male CC57BR mice INS and NAM did not modify the effect of PTZ. Both INS and NAM administered ICB induced short-lasting locomotor excitement in albino SHR and BALB/c mice but not in C57BL/6 or CC57BR mice. Pretreatment with INS (300 mg/kg, IP) prolonged the latency of PTZ seizures only in SHR mice. Pretreatment with NAM was ineffective in all strains tested. Chronic treatment with NAM and INS (100 mg/kg, IP, daily for 5 days) in SHR mice did not modify the effect of PTZ. The data obtained emphasize the importance of the appropriate choice of mouse strain for studies on INS and NAM as puntative endogenous ligands of the BDZ receptor (BDZR). The opposite effects of INS and NAM raise doubts that these two substances could play the same or similar roles in the function of a type of BDZR which is related to the action of PTZ on the central nervous system.
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PMID:Dissimilar effects of nicotinamide and inosine, putative endogenous ligands of the benzodiazepine receptors, on pentylenetetrazol seizures in four strains of mice. 625 61

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 the latency of pentylenetetrazol (PTZ, 500 micrograms iCV) seizures. The same effect was previously observed when PTZ was administered IP. In albino male BALB/c and SHR (bred from Swiss) mice only NA was effective against DL-K. Diazepam in a dose of 0.5 mg/kg prevented PTZ-induced seizures in half of the animals but even in dose of 10 and 20 mg/kg it was ineffective against DL-K. When injected ICV NAM (1 and 10 micrograms), INS (10 micrograms) and HXT (10 micrograms) prevented seizures induced by DL-K and were ineffective against seizures induced by PTZ. It is suggested that if NAM, INS and HXT are of functional importance in the central nervous system, they can act as antagonists of endogenous brain kynurenine. NA and NAM are suggested to be functional feedback inhibitory regulators of the kynurenine pathway of metabolism of tryptophan.
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PMID: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. 626 99

A recently introduced rodenticide containing N-3-pyridylmethyl N'-p-nitrophenyl urea (PNU), Vacor, was accidently ingested by a 25-month-old child, resulting in acute vomiting, lethargy, seizures, and hypoglycemia, as well as chronic evidence of autonomic and peripheral neuropathy and glucose intolerance. Treatment with niacinamide (nicotinamide), may have been of benefit since all problems were resolved within three months of ingestion. This agent (PNU) is remarkably similar chemically and toxicologically to alloxan and streptozocin, both potent beta-cell toxins. These similarities are not only important in regard to the antodite for PNU, but they also suggest that the toxin m,y cause long-term endocrinologic, neurlogic, and oncologic problems.
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PMID:Accidental ingestion of Vacor rodenticide: the symptoms and sequelae in a 25-month-old child. 644 44

The purpose of this study was to investigate the possible importance of adenosine in cerebrocortical vasodilatation accompanying brain activation (epileptic seizures and direct electrical stimulation) and hypoxia (arterial hypoxia and cyanide poisoning of the brain cortex). In chloralose-anesthetized cats a circumscribed area of the brain cortex was treated with adenosine deaminase (Type III; Sigma), which potently deaminates adenosine to the nonvasoactive inosine. Cerebrocortical vascular volume and fluorescence of reduced nicotinamide adenine dinucleotide were measured in vivo by surface fluororeflectometry. The responses of small pial and intracortical vessels to brain activation and hypoxia were studied in brain cortices superfused with artificial (mock) CSF and 5 U/ml adenosine deaminase. It was found that superficially applied adenosine deaminase readily diffuses onto the brain cortex. Prolonged pretreatment of the brain cortices with 0.025 U/ml adenosine deaminase eliminated almost completely the vasodilative effect of 10(-7) mol/ml adenosine. The inhibitory effect of the enzyme on adenosine-induced cortical vasodilatation was specific, because 5 U/ml adenosine deaminase did not attenuate the vasodilative potency of 10(-8) mol/ml 2-chloroadenosine. Adenosine deaminase (5 U/ml) pretreatment of the brain cortices did not diminish the cerebrocortical vascular volume, which increased with arterial hypoxia, topical cyanide poisoning, and direct electrical stimulation. However, it slightly decreased the vasodilative effect of epileptic seizures. On the basis of these results, it seems very unlikely that adenosine is a critical factor in the control of cerebrovascular tone during arterial hypoxia and brain activation.
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PMID:Effect of topical adenosine deaminase treatment on the functional hyperemic and hypoxic responses of cerebrocortical microcirculation. 647 59

The effects of topical inhibition of glycolysis on epilepsy-induced changes of cortical vascular volume (CVV) and fluorescence of reduced nicotinamide adenine dinucleotide (NADH) were investigated in chloralose-anaesthetized cats. CVV and NADH fluorescence were measured by a microscope fluororeflectometer. It was found that 30 min of superfusion of the brain cortex with artificial cerebrospinal fluid (CSF) containing 0.5 mM sodium iodoacetate (IAA) resulted in a 16.4 +/- 0.8% increase in CVV, and 6.6 +/- 0.5% in NADH oxidation. IAA did not alter the electrical activity of the brain cortex. Epileptic seizures in the nonsuperfused brain cortex and following 30 min superfusion of the brain cortex with mock CSF resulted in changes (not significantly different) in CVV and NAD/NADH redox state. They increased CVV and NAD reduction by 28-32% and 7-10%, respectively. Following 0.5 mM IAA treatment of the brain cortex, epileptic seizures led to greatly reduced vascular responses and induced NADH oxidation instead of NAD reduction. Since the topical inhibition of glycolysis reversed the direction of NAD/NADH redox responses accompanying epilepsy, it may be suggested that the relative rate of substrate mobilization as compared with the rate of mitochondrial electron transport is the factor that determines the actual change in NAD-NADH ratio during excessive brain activations. However, contrary to the situation in vitro (isolated mitochondria), the NAD/NADH redox state of the intact brain cortex is not shifted toward oxidation but to reduction during increased electrical activity.
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PMID:Glycolysis and epilepsy-induced changes in cerebrocortical NAD/NADH redox state. 664 11

This study has investigated the feasibility of calculating the cytoplasmic free [NADP+]/[NADPH] ratio in rat brain. The time course of the change in the substrate ratios of the malate dehydrogenase (decarboxylating) [E.C. 1.1.1.40], NADP+-isocitrate dehydrogenase (decarboxylating) [E.C. 1.1.1.42] and 6-phosphogluconate dehydrogenase (decarboxylating) [E.C. 1.1.1.44] reactions was followed for up to 10 min after a single, unmodified electroconvulsive seizure. From the results it has been concluded that during periods of low flux, the direction and magnitude of the change in the cytoplasmic free [NADP+]/[NADPH] ratio can, in fact, be reasonably determined even though there is some uncertainty in the absolute value of the ratio itself. It is recommended that reliance not be placed on a single enzyme system but that one or both of the other systems also be observed under a given experimental condition to increase confidence in the determination. The results also demonstrate that seizure and anoxia have a far lesser effect on the cytoplasmic free [NADP+]/[NADPH] ratio than on the free [NAD+]/[NADH] ratio in the same compartment. These results suggest that the pathways using the nicotinamide-adenine dinucleotide phosphate system are relatively protected from the rapid fluctuations that seizure and anoxia can produce.
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PMID:The calculation of the cytoplasmic free [NADP+]/[NADPH] ratio in brain: effect of electroconvulsive seizure. 679 9

When introduced intracerebroventricularly, quinolinic acid appeared to be the only kynurenine metabolite among those tested (L- and DL-kynurenine sulfate, kynurenic and nicotinic acids, nicotinamide) which induced locomotor excitement and clonic seizures in rats; in high dosage all exhibited convulsant action in mice. L-Kynurenine sulfate (500 micrograms) induced continuous rotation in rats around a longitudinal axis in one or other direction. It also potentiated the convulsant effect of strychnine sulfate and caffeine. Neither the excitatory amino acids, L-glutamic and L-aspartic acids nor the inhibitory amino acids, GABA, glycine and taurine induced excitement or seizures in rats but did in mice. In rats, GABA, glycine and taurine induced sedation, side position and discoordination. The convulsants, strychnine sulfate and pentylenetetrazole, induced seizures both in rats and mice. Differences between species may derive from the better access of intracerebroventricularly administered drugs to mouse hippocampus. Thus mice may be preferable for studies of this type on excitatory amino acids (including kynurenine pathway metabolites) and rats for those on inhibitory amino acids.
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PMID:Excitatory effects of kynurenine and its metabolites, amino acids and convulsants administered into brain ventricles: differences between rats and mice. 713 Sep 75

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 1-aspartic amino acids and inhibitory amino acids GABA, 1-glycine and taurine did not induce either excitation of seizures in rats but did so in mice. Moreover, GABA, 1-glycine and taurine induced obvious sedation, side position and discoordination in rats. Convulsants strychnine sulfate and pentylenetetrazol induced seizures both in rats and in mice. The differences between mice and rats seem to be due to better availability of hippocampus for the intraventricularly administered drugs in mice. Mice seem to be preferable for studies with intraventricularly administered excitatory amino acids including kynurenines, whereas rats are preferable for inhibitory amino acids.
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PMID:[Stimulatory effects of intraventricular administration of kynurenines, amino acids, and convulsants: differences between rats and mice]. 715 52


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