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

Bicuculline-induced status epilepticus was found to be associated with increased amounts of free fatty acids and diacylglycerols in the rat cerebrum. The predominant fatty acid in both lipid pools was arachidonic acid. The accumulation of arachidonoyl-diglycerols decreased at the time of and during behavioral seizures induced by bicuculline, while the amount of free arachidonic acid appeared to increase. We propose a metabolic relationship between these lipids to explain the described changes. The similarities between the composition of the lipid pools and the fatty acid composition of phosphatidylinositol support the hypothesis that these changes may be a result of a convulsion-activated degradation of this phospholipid from excitable membranes.
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PMID:Arachidonic acid and arachidonoyl-diglycerols increase in rat cerebrum during bicuculline-induced status epilepticus. 681 64

The effects of intravenously administered lidocaine on the cerebral cortical energy state and glycolytic metabolism were studied in rats. In one series, rats were divided into five groups according to EEG patterns, i.e., control, desynchronized, synchronized, seizure (1-min duration) and recovery groups. With lidocaine infusion (0.75 mg/min), there were no significant changes from the control group in the cerebral energy state except for a modest increase in phosphocreatine (PCr) in the seizure group and a small decrease in ADP in the non-seizure groups. The cerebral energy charge remained unchanged. Lactate and pyruvate significantly decreased in the non-seizure groups. In a second series, rats were divided into five groups, i.e., control, lidocaine seizure groups (5-min duration, 1.5 mg/min) at hypocapnia, normocapnia and hypercapnia, and a bicuculline (1.2 mg/kg) seizure group. The metabolic changes during lidocaine seizure were essentially the same as those observed in the seizure group in the first series. However, the increase in PCr during lidocaine seizure was significant only in the hypocapnic and the normocapnic groups. Bicuculline-induced seizures were accompanied by a significant decrease in high energy phosphates. In summary, neither a non-seizure nor-seizure dose of lidocaine caused any reduction in the cerebral energy charge nor was there any evidence of increased anaerobic metabolism in the cerebral cortex during lidocaine-induced seizures.
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PMID:Cerebral energy state and glycolytic metabolism during lidocaine infusion in the rat. 721 27

The effects of some gamma-aminobutyric acid (GABA) antagonists and other "convulsants" have been tested on neurones of the isolated olfactory cortex slice preparation of the guinea-pig using single cell intracellular and gross extracellular recording techniques. Bicuculline, picrotoxin, strychnine, leptazol, bemegride, and also theophylline and d-tubocurarine all increased the duration and amplitude of the excitatory postsynaptic potential, thereby producing a seizure-like discharge. These drugs reduced and shortened the peak conductance increase during the inhibitory postsynaptic potential (i.p.s.p.) in normal solution and after the i.p.s.p. had been prolonged by the presence of a barbiturate. The results suggested that these drugs antagonise synaptic inhibition through a common mechanism, perhaps by reducing the effect of neurally released GABA.
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PMID:Convulsants antagonise inhibition in the olfactory cortex slice. 744 24

1. The effects of some GABAergic and dopaminergic agents on pyrimethamine-induced tonic seizures were investigated in mice. 2. Pyrimethamine dose dependently induced seizures in mice. 3. Muscimol, AOAA and DABA significantly protected mice against pyrimethamine-induced seizures. 4. Bicuculline and picrotoxin effectively potentiated seizures elicited by pyrimethamine and significantly antagonized the protective effect of muscimol against the seizures. 5. Diazepam and phenobarbitone effectively protected mice against seizures elicited by pyrimethamine. 6. L-Dopa significantly potentiated pyrimethamine-induced seizures. 7. Apomorphine and pargyline significantly reduced the latency of seizures induced by pyrimethamine. 8. Haloperidol and pimozide effectively protected mice against pyrimethamine-elicited seizures and also significantly antagonized the potentiating effects of apomorphine and L-dopa on the seizures. 9. Disulfiram significantly potentiated seizures induced by pyrimethamine and also significantly enhanced the seizure-potentiating effect of L-dopa. 10. alpha-Methyl-p-tyrosine effectively protected against seizures induced by pyrimethamine. However, L-dopa significantly potentiated the seizures in alpha-methyl-p-tyrosine-pretreated animals. 11. Muscimol significantly attenuated the potentiating effect of L-dopa on pyrimethamine-induced seizures while bicuculline significantly enhanced the effect of L-dopa. Furthermore, haloperidol significantly potentiated the protective effect of muscimol against pyrimethamine-induced seizures. 12. These results suggest that both GABA and dopamine might be involved in the mechanism(s) of pyrimethamine seizures in mice.
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PMID:GABAergic and dopaminergic systems may be involved in seizures induced by pyrimethamine in mice. 787 56

Bicuculline is an antagonist of gamma-aminobutyric acid (GABA) receptors, and muscimol is an agonist of GABA receptors. In this study, the effects of bilateral injections of bicuculline and muscimol into the caudate-putamen (CP) were compared in amygdaloid-kindled rats. Thirty minutes after the injection of bicuculline (1, 10 and 100 pmol per CP) or muscimol (10, 50 and 100 nmol per CP), the kindled amygdala was stimulated at the previously established generalized seizure triggering threshold (GST). Most doses of bicuculline caused no significant alteration either in the seizure stage or in the afterdischarge duration. Only the 100-pmol dose produced a marked reduction in the afterdischarge duration. With 10 nmol of muscimol, there was no significant change in the kindled seizure stage or in the afterdischarge duration. However, 50 and 100 nmol of muscimol markedly suppressed both parameters. These findings suggest that CP efferent pathways are involved in the mechanism that underlies the development of kindled amygdaloid seizures, and support the concept that GABA acts as an anticonvulsant in the brain.
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PMID:Comparison of effects of bilateral injections of bicuculline and muscimol into the caudate-putamen of amygdaloid-kindled rats. 804 67

The effects of muscimol, amino-oxyacetic acid (AOAA), diamino-N-butyric acid (DABA), bicuculline, picrotoxin, diazepam and phenobarbitone on the protective effect of clonidine against pentylenetetrazol-induced seizures were studied in mice. Muscimol, AOAA, DABA, phenobarbitone and diazepam significantly protected mice against pentylenetetrazol-induced seizures and also significantly potentiated the protective effect of clonidine against the seizures. Bicuculline and picrotoxin significantly potentiated seizures induced by pentylenetetrazol and significantly attenuated both the protective effects of muscimol and clonidine against the seizures. These data suggest that activation of gamma-aminobutyric acid systems may underlie the protective effect of clonidine against seizures induced by pentylenetetrazol in mice.
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PMID:gamma Aminobutyric acid mediation of the anticonvulsant effect of clonidine on pentylenetetrazol-induced seizures in mice. 805 98

The effects of muscimol, aminooxyacetic acid (AOAA), diamino-n-butyric acid (DABA), baclofen, bicuculline, picrotoxin, strychnine, diazepam, phenobarbitone and phenytoin on cimetidine-induced seizures were studied in mice. Cimetidine (400-1000 mg/kg, i.p.) induced dose-dependent tonic convulsion. Muscimol, AOAA and DABA effectively protected mice against cimetidine-induced seizures. Bicuculline and picrotoxin significantly potentiated the seizures induced by cimetidine and effectively antagonized the protective effects of muscimol, AOAA and DABA against the seizures. Diazepam and phenobarbitone significantly protected the mice against cimetidine-induced seizures while phenytoin and strychnine did not significantly alter the seizures. These results indicate that the attenuation of central gamma-aminobutyric acid neurotransmission may underlie cimetidine-induced seizures in mice.
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PMID:Cimetidine-induced seizures in mice. Antagonism by some GABAergic agents. 827 50

Changes in the GABAergic system after chronic treatment with bicuculline were examined in two strains of inbred rats, Fischer 344 (F344) and Lewis (LEW). Rats received an IP injection of either bicuculline (2 mg/kg) or vehicle once a day for 12 days. After this chronic treatment, the effects of diazepam (1 mg/kg, IP) and pentobarbital (20 mg/kg, IP) on bicuculline-induced convulsions were measured. Bicuculline was acutely infused into a tail vein at 0.0415 mg/min, and the infusion was terminated when rats showed seizure. Following the chronic bicuculline treatment, the anticonvulsant effect of diazepam, but not of pentobarbital, was significantly reduced as compared to its effect following chronic vehicle treatment in both strains. Both diazepam and pentobarbital showed a significant difference in anticonvulsant effects between strains (F344 > LEW). The hypnotic effects of muscimol, barbital, pentobarbital, and ethanol following chronic bicuculline treatment were examined. There was no significant difference in sleep time induced by these drugs between bicuculline- and vehicle-treated rats. These results suggest that the attenuation of diazepam's anticonvulsant effect after chronic bicuculline treatment may result from functional changes in benzodiazepine receptors and that the anticonvulsant effects of diazepam and pentobarbital may be influenced by genetic factors. Moreover, the hypnotic effects of several drugs tested are apparently not affected by chronic bicuculline treatment.
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PMID:Attenuation of anticonvulsant effects of diazepam after chronic treatment with bicuculline. 841 27

A novel method for the assessment of the threshold for clonic seizures induced by excitatory amino acids based on continuous infusion of the glutamate agonists [alpha-amino-3-hydroxy-5-terbutyl-4-isoxazolepropionate (ATPA), kainate or N-methyl-D-aspartate (NMDA)] into the lateral brain ventricle of unrestrained mice is reported. Using this novel method of seizure threshold determination, it was found that systemically administered diphenylhydantoin and carbamazepine elevated the threshold for ATPA and had negligible effects on the threshold for kainate and NMDA. Phenobarbital and trimethadione elevated the threshold for all excitatory amino acids tested, whereas valproate elevated the threshold for ATPA and kainate seizures. Ethosuximide elevated the threshold for ATPA and kainate and decreased the threshold for NMDA seizures. The quisqualate antagonists [2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline and 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine] elevated the threshold for ATPA and less so for kainate seizures, whereas the NMDA antagonist 3-((+-)2-carboxypiperazine-4-yl)-propyl-1-phosphonate elevated the threshold for NMDA seizures. 1-(4-Aminophenyl)4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine in higher doses was also active against NMDA seizures, whereas 3-((+-)2-carboxypiperazine-4-yl)-propyl-1-phosphonate did so with kainate seizures. Among seven different convulsants, pentylenetetrazol, picrotoxin and the beta-carboline methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate lowered the threshold for seizures induced by excitatory amino acids. Pentylenetetrazol and picrotoxin did so with kainate seizures, whereas methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate lowered ATPA thresholds. Bicuculline, 3-mercaptopropionate, strychnine and pilocarpine were inactive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of the seizure threshold for excitatory amino acids in mice by antiepileptic drugs and chemoconvulsants. 850 95

Experiments were aimed at assessing a possible different sensitiveness to seizures in aggressive vs. nonaggressive rates. Thirty-nine muricidal rats were selected by using a sedated mouse. Six of these killer rats (K) showed electroencephalographic (EEG) spontaneous syncronous wave-and-spike discharges, 6-11 c/s. None of nonkiller animals (NK) showed a similar pattern. These 6 K were not used for the subsequent experiments. Intraperitoneal pentylentetrazole (PTZ; 10, 20, and 40 mg/kg) or bicuculline (BIC; 2 and 4 mg/kg) was given to both NK and K. K were more sensitive than NK to the epileptogenic effects of 20 mg/kg PTZ and 2 mg/kg BIC, as revealed by the significant increased number of convulsive rats and longer duration of EEG seizures. No difference in EEG or convulsant behavior was observed between K and NK after the administration of the lower dose of PTZ and the high dose of PTZ or BIC. The use of K rats as a possible new sensitive model of petit mal is discussed.
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PMID:Is there a relationship between rat latent aggressiveness and susceptibility to convulsive crises? 877 67


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