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)

In electroshock test apomorphine appeared without effect, D, L-amphetamine and L-DOPA (in a high dose) elevated the convulsive threshold, while amantadine decreased it. Among investigated dopamine (DA) receptor blockers spiperone, pimozide and fluphenazine lowered the threshold, haloperidol being without effect. The convulsive threshold elevated by L-DOPA was not affected by neuroleptics and phentolamine but on the other hand DA receptor blockers and phentolamine anatagonized the effect of D, L-amphetamine. The effect of amantadine was not influenced by neuroleptics. In pentylenetetrazol (PTZ) test only amantadine and L-DOPA (in high doses) affected the threshold, increasing seizure susceptibility; the above effect was not abolished by pimozide. Our results seem to indicate that the activity of brain DA system seems not to be involved directly in the susceptibility to electrogenic or PTZ-induced seizures in mice.
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PMID:Brain dopamine and seizure susceptibility in mice. 74 May 53

In experiments with pentylenetetrazol convulsion model it has been found that L-DOPA in a dose of 50 mg/kg has no influence, while 500 mg/kg potentiate convulsions. Amantadine in a dose of 25 mg/kg and particularly markedly in a dose of 100 mg/kg potentaites convulsive seizures. Amphetamine in a dose of 0.5 mg/kg has no effect, while 5 mg/kg potentiate convulsive seizures, which is particularly pronounced in mice. Apomorphine in doses of 0.5 and 5 mg/kg has no marked effect on convulsions. Haloperidol in doses of 0.2 and 2 mg/kg does not have a pronounced effect on convulsive-seizure reactions and does not influence the effect of L-DOPA and amantadine on these reactions. The results obtained suggested a rather indirect effect of the dopaminergic system on convulsive-seizure reactivity. It is possible that the effects of some of the dopaminergic agents studied are realized through influencing the relationships between the dopaminergic system and other neurotransmitter systems (especially cholinergic, GABA-ergic and serotonin-ergic).
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PMID:On certain effects of dopaminergic agents in pentylenetetrazol convulsions. 75 52

1 The behavioural effects induced by histidine were studied in two species. In rabbits, sedation was assessed by the presence of blepharospasm, loss of righting reflex, and loss of response to painful stimuli. In mice, sedation and arousal were assessed by changes in the locomotor activity, exploratory activity, and minimal electroshock seizure threshold.2 The administration of histidine to normal rabbits or mice, in doses of 800 mg/kg and 1000 mg/kg respectively, had no apparent effect on behaviour. Moreover, it did not affect the behavioural excitation induced by L-DOPA (100 mg/kg i.v. in rabbits and 750 mg/kg i.p. in mice) in these animals.3 The administration of histidine with or after L-DOPA in reserpine-treated rabbits (2.5 mg/kg i.v.) or mice (5 mg/kg, i.p.) produced sedation. This sedative effect was dose-dependent.4 The sedative effects induced by histidine after DOPA-induced arousal in reserpine-treated rabbits and mice were prevented by prior injection of the histamine H(1)-receptor blockers, chlorpheniramine (2.5 mg/kg) or diphenhydramine (5 mg/kg).5 Imipramine (7 to 10 mg/kg, i.v.)-induced arousal in reserpine-treated rabbits was also reversed by histidine infusion.6 The infusion of 5-hydroxytryptophan (100 mg/kg, i.v.) with L-DOPA, or of arginine (450 mg/kg, i.v.) with or after L-DOPA, or of histamine (100 mug/kg), i.v.) after L-DOPA, did not affect the DOPA-induced arousal in reserpine-treated rabbits.7 These findings indicate that histamine, formed centrally from exogenous histidine, and released in increased amounts at the synapses in reserpine-treated animals, possesses a central sedative effect. This effect may be sufficient to antagonize the behavioural excitation induced by high levels of catecholamines in the brain of these animals when aroused by L-DOPA administration.8 It is concluded that in addition to the other monoamines, histamine may also be implicated in the regulation of brain excitability.
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PMID:Reversal of DOPA-induced arousal in reserpine-treated rabbits and mice by histidine. 76 Sep 4

The increasing number of latent and manifest hyperuricemia is important concerning differential diagnosis in neurological and psychiatric diseases. The pathological importance of hyperuricemia in these diseases is particularly unknown. The possibility of a physiological regulative function of uric acid in central nervous system may be discussed. Therefore uric acid typing in cerebrospinal fluid were made of 173 patients with neurological and psychiatric diseases. On an average the uric acid level in cerebrospinal fluid is 1:10 of the blood uric acid level. In advanced age a lower level could be found. High level for example were found after L-Dopa treatment and epileptical seizures. These results and possible pathophysiological correlation to the correspondant diseases are discussed.
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PMID:Typing of uric acid level in cerebrospinal fluid in neurological and psychiatric diseases. 85 22

Mice with a genetically determined susceptibility to audiogenic seizures were utilized to analyze the ontogeny of central monoamine neurotransmission in relation to a behavior with age-specific properties. Levels of noradrenaline (NA), dopamine (DA), and 5-hydroxytryptamine (5-HT) were measured in forebrain and hindbrain regions at 14, 21, 28, and 42 days postnatal age in genetically sensitive or resistant strains of mice. An in vivo estimate of tyrosine and tryptophan hydroxylase activity was obtained at the same ages by following the accumulation of 3,4-dihydroxyphenylalanine (DOPA) and 5-hydroxytryptophan (5-HTP) respectively, after the administration of a centrally effective L-amino acid decarboxylase inhibitor (R04-4602, 800 mg/kg). At 14 days, there was a faster rate of accumulation of DOPA in both the forebrain and hindbrain of the sensitive mice compared to mice of the nonsensitive strain. At 21 days, the age of maximal sensitivity in the sensitive mice, the levels of NA were significantly lower in both regions of the sensitive mice, but the accumulation of DOPA was similar between strains at this age. There was also a slightly lower level of 5-HT in the forebrain of sensitive mice at 21 days accompanied by a slower rate of accumulation of 5-HTP in this region. In the hindbrain of the sensitive animals however, the rate of accumulation of 5-HTP was faster than in the sensitive strain. At 28 days, some impairment in mechanisms within NA-containing neurons in the sensitive mice was still apparent (including lower NA levels). At 42 days, there were no differences in amine levels, however, the levels of accumulated DOPA and 5-HTP were significantly lower in the sensitive strain. The results suggest that in the sensitive mice, developmental differences in mechanisms of monoamine storage and/or synthesis may exist which could contribute to deficient amounts of physiologically releaseable transmitter.
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PMID:Audiogenic seizures: relation to age and mechanisms of monoamine neurotransmission. 108 62

Duration of postictal coma following maximal electroshock seizure and monoamine levels in the whole brain were measured in mice. Pretreatment with intraperitoneal alpha-methyl-p-tyrosine (alpha-MT), 5-hydroxytryptophane (5-HTP), or intraventricular 6-hydroxydopamine (6-OHDA) prolonged the coma duration, whereas p-chlorophenylalanine (PCPA) did not affect the coma, and L-DOPA tended to shorten the coma and counteracted the effect of alpha-MT. When the shock was repeated five times with one hour intervals, the duration of coma was progressively increased being accompanied by elevated serotonin (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) levels in the brain. In alpha-MT treated group, a striking parallelism was remarked between coma prolongation and norepinephrine (NE) or dopamine (DA) reduction. These data suggest that prolongation of postictal coma is correlated with reduced NE and DA levels and/or with elevated 5-HT and 5-HIAA levels in the brain.
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PMID:Correlation between brain monoamine levels and postictal coma following electroshock. 115 19

Spontaneously hypertensive rats (SHR) were compared with normotensive Wistar rats for their sensitivity to tonic extensor seizures. SHR were more sensitive to seizures and did not respond to the anticonvulsant effects of L-DOPA. SHR had a slower turnover rate of norepinephrine in brain stem and cortex and of dopamine in striatum. Steady-state levels of catecholamines were similar in both groups. These findings are consistent with earlier ones that reported an inverse relationship between central catecholamine activity and sensitivity to electroconvulsive seizures.
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PMID:Increased susceptibility to seizures and decreased catecholamine turnover in spontaneously hypertensive rats. 118 83

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

A case of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes, in which a pituitary growth hormone (GH) secretion deficiency of hypothalamic origin was revealed through neuro-endocrinological examinations, was described. The case was a 10-year-old girl, who had been suffering from generalized tonic seizures since age 5, four episodes of alternating hemiplegia since age 6, stunted growth since age 7, and simple partial motor seizures as well as gelastic seizures since age 8. Marked elevation of lactate and pyruvate in both serum and CSF, abundant ragged red fibers in biopsied muscle, and low density areas in the left occipital lobe and bilateral globus pallidus in addition to diffuse brain atrophy on CT scan and MRI of the head were demonstrated, although the activities of muscle enzymes complex I-IV were within normal ranges. Pituitary GH secretion was deficient under the loadings with insulin, L-DOPA, sleep, and a single growth hormone releasing factor (GRF) administration, but normal GH response was registered under the repetitive stimulation with GRF. Activities of other hormonal axes were normal. It is likely that short stature commonly observed in MELAS patients is due to hypothalamic dysfunction, which might be brought out by chronic ischemia and energy deficiency of the diencephalon based upon mitochondrial abnormality of that region. It is likely that gelastic seizure in this case is due to hypothalamic dysfunction.
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PMID:[Hypothalamic GH Deficiency and gelastic seizures in a 10-year-old girl with MELAS]. 187 57

Influences of the manipulation of brain catecholaminergic neuronal activity on the incidence of lidocaine-induced convulsions in mice were studied and compared with those of pentylenetetrazol (PTZ)-induced convulsions. alpha-Methyl-p-tyrosine (alpha-MPT) decreased both brain noradrenaline (NA) and dopamine (DA) levels, and disulfiram decreased the NA level and increased the DA level. The incidence of lidocaine-induced convulsions was decreased by treatments with alpha-MPT and disulfiram, while that of PTZ was increased by either treatment. The incidence of lidocaine-induced convulsions was slightly, but not significantly increased by L-dihydroxyphenylalanine (L-DOPA), although the brain DA level was increased by L-DOPA. Methamphetamine and desipramine increased the incidences of lidocaine-induced convulsions. These results may suggest that brain catecholaminergic neurons, differing from their role in inhibiting control of PTZ-seizure, act to facilitate lidocaine-induced convulsions.
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PMID:Changes in convulsion susceptibility of lidocaine by alteration of brain catecholaminergic functions. 188 Sep 90


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