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

A series of ergot alkaloids, together with the DA agonists apomorphine and piribedil, were tested for protective effects against audiogenic seizures in an inbred strain of mice (DBA/2) and for induction of circling behaviour in mice with unilateral destruction of one nigrostriatal DA pathway. The order of potency against audiogenic seizures was apomorphine greater than ergocornine greater than bromocryptine greater than ergometrine greater than LSD greater than methysergide greater than piribedil while that observed in the rotating mouse model was apomorphine greater than ergometrine greater than ergocornine greater than bromocryptine greater than piribedil. LSD caused only weak circling behaviour even when administered in high doses (greater than 1 mg/kg). Methysergide was ineffective. Prior administration of the neuroleptic agent haloperidol blocked the effect of DA agonists and of ergot alkaloids in both animal models. The possible action of ergot alkaloids as DA agonists is discussed.
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PMID:Ergot alkaloids as dopamine agonists: comparison in two rodent models. 98 4

C57 and DBA mice whose parents had been fed alcohol were more susceptible to audiogenic seizures and had a shorter latency to seizure than either pair-fed or normally fed controls.
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PMID:Audiogenic seizures in mice whose parents drank alcohol. 100 72

The degree of audiogenic seizure was measured in DBA/2J (phenylalanine hydroxylase deficient) mice as a function of dietary phenylalanine (Phe) and injected 5-hydroxytryptophan (5-HTP), the precursor of serotonin (5-HT). Phe was shown to exacerbate seizures significantly, and seizure severity was found to be directly related to dietary concentration when animals were not treated with exogenous 5-HTP. 5-htp was observed to significantly ameliorate seizures. The seizure-intensifying effect of Phe was reversible by 5-HTP injection and protection against seizures was directly related to 5-HTP concentration for animals on a high Phe diet. The results of this study indicate that Phe and 5-HTP are mutually antagonistic in modulating audiogenic seizure suceptibility.
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PMID:Effects of phenylalanine and 5-hydroxytryptophan on seizure severity in mice. 108 44

6-Methoxy-1, 2, 3, 4, -tetrahydro-beta-carboline (6-MeO-THBC) was tested for anticonvulsant properties against audiogenic seizures in DBA/2J and primed C57BL/6J mice (i.e., mice given a prior auditory exposure) and aginast electroconvulsive seizures in DBA/2J mice. 6-MeO-THBC (100 mg/kg) was found to attenuate both types of behavioral seizures 2 hr after injection as compared to saline controls. In addition, 6-MeO-THBC increased whole brain serotonin and decreased whole brain 5-hydroxyindoleacetic acid 2 hr after injection. These results support previous reports which suggest a serotonergic involvement in behavioral seizures.
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PMID:Anticonvulsant effects of 6-methoxy-1, 2, 3, 4-tetrahydro-alpha-carboline on audiogenic and electroconvulsive seizures in mice. 112 56

Susceptibility to audiogenic seizures has been produced in otherwise non-susceptible mice by acoustic stress and by conductive hearing loss. Both procedures temporarily elevate the absolute threshold of the auditory evoked potential (AEP) and are maximally effective during a circumscribed period of early development. In the genetically SUSCEPTIBLE DBA/2J mouse, AEP thresholds indicated that its auditory system is functionally less mature during this early period than that of the nonsusceptible C57BL/6Jmouse. It was proposed that innate susceptibility found in the DBA/2J mouse results from auditory disuse supersensitivity during a critical developmental period, in support of Saunders' hypothesis for acoustically primed mice. The increased peak-to-peak AEP amplitudes, however, were not believed to be causally related to the audiogenic seizures.
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PMID:Auditory similarities associated with genetic and experimental acoustic deprivation. 115 Sep 63

The effects of pyridoxine deficiency and the administration of supplemental vitamin B6 on audiogenic and electroconvulsive seizures were studied in two inbred strains of mice and their F1 hybrids. Pyridoxine deficient diets increased seizure risk, whereas supplemental vitamin B6 protected these animals against seizures. Penicillamine and thiosemicarbazide, at doses which lowered brain levels of pyridoxine by only 10%, increased seizure risk. Diets deficient in zinc and copper did not alter susceptibility to either audiogenic or electroconvulsive seizures. DBA/2J mice, genetically susceptible to audiogenic seizures, have the same endogenous levels of pyridoxine in the brain as do C57Bl/6J mice, which are resistant to audiogenic seizures.
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PMID:Levels of pyridoxine and susceptibility to electroconvulsive and audiogenic seizures. 117 97

Audiogenic seizures in DBA/2 mice have been studied after administration of drugs believed to act as dopamine agonists. Apomorphine at 0.4 mg/kg delays all phases of the response, the tonic phase is absent after 2.0 mg/kg; the clonic phase is abolished by 10 mg/kg. Ergocornine (0.5-8.0 mg/kg) produces effects on the latency and occurrence of seizure stages similar to those of apomorphine. Piribedil, ET 495 (4-100 mg/kg) is less potent; even after 100 mg/kg clonic and tonic phases occurred in 50% of the mice.
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PMID:Effects of apomorphine, ergocornine and piribedil on audiogenic seizures in DBA/2 mice. 117 46

The activities of catechol-O-methyl transferase (COMT), monoamine oxidase (MAO), and a methanol forming enzyme were studied in whole brain homogenates and in livers obtained from DBA/2J, C57B1/6J, and F1 hybrid mice. DBA/2J mice are extremely susceptible to audiogenic seizures, whereas C57B1/6J mice are resistant to sound-induced convulsions. C57B1/6J mice were found to have significantly higher brain levels of COMT, while MAO activities were not different in animals of these genotypes. No methanol forming activity was detected in animals of either strain. No differences were found in hepatic activities of either COMT or MAO. Pyrogallol was shown to protect DBA/2J animals against audiogenic seizures.
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PMID:Catechol-O-methyl transferase and monoamine oxidase activities in brains of mice susceptible and resistant to audiogenic seizures. 118 92

Genetically seizure susceptible DBA/1/Bg mice fed 10% ethanol in their drinking water exhibited a marked diurnal variation in blood alcohol levels. At peak levels, sound-induced seizures were significantly reduced. At trough levels, seizures remained unaffected. Ethanol administered during early development enhanced seizures at post-weaning age. Such alcohol-augmented seizures were suppressed by ethanol feeding during the testing period, to the same base level as in animals not pretreated with ethanol in early life.
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PMID:Suppressant effects of alcohol on audiogenic seizures. 123 99

Tryptophan hydroxylase (TPH) activity was determined in whole brain from male C57BL/10/Bg and DBA/1Bg mice at 14 different ages between postnatal days 4 and 33. Brain TPH activity was higher at every age in C57BL/10/Bg than in DBA/1/Bg mice, the difference being 30-50% after day 20. The apparent Km of the enzyme for substrate was identical (1.4 X 10(-5) M) in both strains. The reciprocal F1's between DBA/1/Bg and C57BL/10/Bg strains were similar in TPH activity, being slighlty lower than the predicted midparental value. At 30 days of age, C57BL/6/Bg males also had high TPH activity, indistinguishable from the C57BL/10/Bg strain. Audiogenic seizure susceptibility in these strains and their hybrid F1's was inversely correlated with their brain TPH activities. These results indicate that seizure susceptibility and aggression in mice may be related to the serotonergic activity in the brain. In the case of seizures, ethanol-induced susceptibility to audiogenic seizures in mice was enhanced by reserpine, and the effect of reserpine could be reversed by 5-HTP but not by DOPA. Furthermore, p-chlorophenylalanine also enhanced such susceptibility, whereas alpha-methyltyrosine had no effect. In the withdrawal audiogenic seizures in mice during chronic ethanol treatment, adrenalectomy blocked the ethanol-induced increase of brain TPH activity and also prevented the withdrawal seizures. Our results are consistent with the hypothesis that the serotonergic system is among the components regulating excitability in the brain.
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PMID:Pharmacogenetic studies of the serotonergic system in association with convulsive seizures in mice. 124 14


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