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)

A convulsant dose (100 mg/kg) of l-methionine-RS-sulphoximine (MSO) produced temporally correlated decreases in central 5-hydroxytryptamine (5-HT) and plasma and brain tryptophan (TRY) concentrations in C57BL/6J mice. In contrast, a subconvulsant dose of MSO (50 mg/kg) had no effect on central 5-HT levels and only decreased brain tryptophan at one time-point after its administration. The pattern of findings suggests that the decrease in central 5-HT levels resulting from a convulsant dose of MSO is related to an impairment in 5-HT synthesis resulting from a restriction of tryptophan availability. Administration of 25 mg/kg and 100 mg/kg doses of l-tryptophan with convulsant doses of MSO significantly increased seizure latency. It is suggested that the central 5-HT system modulates the expression of MSO-induced seizures.
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PMID:Tryptophan availability, central serotonergic function and methionine sulphoximine-induced convulsions. 706 6

The opioid peptides Leu-enkephalin, Met-enkephalin and D-Ala2-Met-enkephalinamide were injected at various concentrations into the neocortex and hippocampus of rats to examine their effects on EEG activity and DC potentials. All three compounds were found to elicit spreading depression (SD) in both structures. Higher doses of Met-enkephalin were required to elicit SD as well as seizure activity. In the hippocampus the wave of SD was frequently preceded by seizure activity which was antagonized by naloxone pretreatment (40 mg/kg i.p.). Naloxone also prevented Leu-enkephalin-induced SD in the neocortex (but not in the hippocampus) and Met-enkephalin-induced SD in the hippocampus (but not in the neocortex). It failed to block SD elicited by D-Ala2-Met-enkephalinamide in both structures. Some of the various reported behavioral effects of intracranial injections of enkephalins could be artefacts of hippocampal and/or cortical spreading depression.
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PMID:Spreading depression induced by microinjection of enkephalins into the hippocampus and neocortex. 722 10

FK-33,824 (Tyr-D-Ala-Gly-MePhe-Met(O)-ol) and metkephamid (Tyr-D-Ala-Gly-Phe-N(Me)Met-CONH2; LY 127623) are two parenterally active synthetic analogues of the endogenous morphinomimetic pentapeptide, [Met5]-enkephalin. Acute s.c. administration of each analogue raised the seizure threshold in a dose-related manner in rats challenged with flurothyl, a volatile convulsant. The anticonvulsant action was antagonized by a low dose of naloxone (0.10 mg/kg s.c.). FK-33,824 and metkephamid can therefore be classified with typical mu-receptor agonists such as morphine and etorphine in this procedure.
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PMID:A comparison of the anticonvulsant effects of two systemically active enkephalin analogues in rats. 723 80

Brain content of leucine-enkephalin and methionine-enkephalin changes independently during kindling of the amygdala. Both peptides were measured after 4, 8, 15 and 21 days of stimulation. Leu-enkephalin showed a progressive increase during the kindling: the results on the 4th day did not differ significantly from the controls, whereas those on the 8th day displayed an increase only in the stimulated left hemisphere and those on the 15th day showed an increase in both hemispheres. This increase was also seen after 21 days of stimulation. In contrast, Met-enkephalin was not modified during the early stages of kindling, but was found to be increased after the animals had presented five or more generalized seizures. These results show that Leu-enkephalin is related to the development of kindling, whereas Met-enkephalin levels change only as a consequence of the generalized seizures.
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PMID:Brain content of leu5- and met5-enkephalin changes independently during the development of kindling in the rat. 730 Dec

The aminoacid content of cerebrospinal fluid (CSF) was studied in 51 patients with the epileptic syndrome in conjunction with tumors and cerebral arachnoiditis. In general epileptical seizures CSF demonstrated the highest glutamine content. A drop in the glutamine concentration was seen in hydrocephalus, in rare general and focal seizures. The epileptic syndrome is characterized by an increase in CSF of cystidin, thyrosine and methionine. More pronounced changes in aminoacid metabolism were detected in the epileptic syndrome, in chronic inflammatory brain disorders.
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PMID:[Amino acid composition of cerebrospinal fluid in the epilepsy syndrome]. 741 7

We previously suggested that a deficit of anticonvulsant endogenous methionine enkephalin, in the cerebral cortex, septal area, hippocampus, and striatum of seizure-susceptible El mice plays a role in the pathogenesis of seizures. To determine whether a hypofunction of enkephalinergic neuron may be due to metabolic abnormalities of opioid peptides in the El mouse brain, we measured methionine enkephalin-like immunoreactivity (ME-LI) of 50 fractions eluted by high performance liquid chromatography obtained from those four regions of the brain of El and seizure-nonsusceptible ddY mice (the mother strain of El mice). We observed the same ME-LI patterns of 50 fractions in the cerebral cortex and septal area in El and ddY mice, whereas exhibited differing ME-LI patterns in the hippocampus and striatum in the two stains. Different ME-LI patterns may imply the difference in the metabolic profile of opioid peptides. Thus, an abnormal metabolism of opioid peptides in the hippocampus and striatum of the El mouse may be involved in the pathogenesis of seizures.
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PMID:Metabolic profile of opioid peptides differs in the hippocampus and striatum of seizure-susceptible E1 mice. 760 26

Volatile anaesthetics (VAs) act essentially as central nervous system (CNS) depressants. However, many evidences obviously demonstrate that VAs are also CNS excitants. In this review, we adduce our previous studies which are relevant to the behavioural evidences of the CNS excitation actions of VAs. Anaesthetic-induced opisthotonus (OP) found in mice is thought to be a sign of CNS stimulation and the order of the incidence inversely coincides with that of blood/gas partition coefficient, that is, the smaller the coefficient, the higher the incidence of OP as far as the halogenated ether anaesthetics are concerned. In other words, the shorter the induction time to anaesthesia, the greater the incidence. A striking observation is that the incidence due to isoflurane is much higher than that to enflurane, while in humans, enflurane often produces convulsion whereas isoflurane when administered alone has not been found to cause electroencephalographic or clinical seizures in anaesthetized patients. We also found that enflurane-induced OP is possibly mediated by N-methyl-D-aspartate- and glycine-receptor but not GABAA-receptor and that the intensity of immunoreactivity of methionine-enkephalin in hippocampal mossy fibre is well correlated with the incidence among three strains of mice. We demonstrated that the open-field activity in ddN mice significantly increased on and after emergence from anaesthesia with enflurane and isoflurane. The effect of very low concentrations of halothane, enflurane and isoflurane on acquired active avoidance training was assessed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Volatile anaesthetics as central nervous system excitants. 771 Feb 23

The changes of opioid peptide reactivity in seizure activity have been well studied in animals. Increased enkephalin and dynorphin immunoreactivity in the hippocampi of animals are interpreted as the result of seizure induced mossy fibre sprouting. We studied the hippocampi of six patients with a history of long-standing grand mal seizures and six age-matched control patients with no history of epilepsy or neurologic disease, using frozen sections which were immunostained with antibodies against Leu-enkephalin and Met-enkephalin. The staining intensity in the CA3, CA4 and internal molecular layer of the dentate fascia in each case was quantified using optical densitometry image analysis. The CA3 and CA4 of the epileptic hippocampi showed highly significant increase in Leu-enkephalin-like immunoreactivity compared to the controls (P < 0.005) while the inner molecular layer showed only significant increase (P < 0.05). Met-Enkephalin-like immunoreactivity was only significantly increased in CA4 of the epileptic hippocampi (P < 0.05).
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PMID:Increase in enkephalin-like immunoreactivity in hippocampi of adults with generalized epilepsy. 795 7

Serum amino acid (AA) profiles are altered in epilepsy. It is not clear whether this is due to the disease process itself or to other variables such as seizure type, seizure frequency, duration of illness, medication, or altered liver function. We investigated serum AA profiles and liver enzymes in 73 epileptic patients and 90 healthy subjects and evaluated the data by analysis of variance to discriminate between age, sex, seizure type, duration of illness, seizure frequency, antiepileptic drug (AED) and increased serum liver enzyme levels, and their putative interaction with the serum AA profile. There was no correlation between the changes in the AA profile and age, duration of illness, seizure frequency, and seizure type. Seventy-two percent of the AED-treated patients and 33% of the unmedicated patients showed an increase in one or several serum liver enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), and/or gamma-glutamyl transferase (gamma-GT)]; particularly gamma-GT. We observed a significant increase in serum concentrations of glutamine and glycine and decreased levels of taurine, threonine, serine, valine, methionine, isoleucine, leucine, phenylalanine, histidine, tryptophan, and arginine in AED-treated patients but not in unmedicated patients. These results show that the changes in the serum AA profiles of epileptic patients treated with AEDs occur in patients with alteration of serum liver enzymes; whether this implies a causal relation is still uncertain.
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PMID:Serum amino acids, liver status, and antiepileptic drug therapy in epilepsy. 809 92

Pretreatment of mice with 5-fluoromethylornithine (5FMOrn), a selective inactivator of ornithine aminotransferase, diminishes the accumulation of ammonia in the brain after administration of ammonium acetate, and antagonizes ammonia-induced fatal tonic extensor convulsions. In about 50% of the treated animals the loss of the righting reflex and coma is prevented. Presumably these effects are based on the enhancement of urea formation by the increased liver ornithine concentrations. However, since brain ornithine concentrations are greatly enhanced by 5FMOrn, it is not excluded that ornithine has direct effects on cellular events involved in ammonia-induced seizure generation, even though 5FMOrn had no anticonvulsant properties in a series of established animal seizure models, including N-methyl-D,L-aspartate-induced convulsions. NMDA receptor antagonists are capable of preventing death, but do not protect against the generation of coma and tonic extensor convulsions in ammonium acetate intoxicated mice. Since no evidence was found for ammonia-induced glutamate release from rat hippocampus, there is no convincing evidence for the idea that the tonic convulsions are mediated by NMDA receptors. L-Methionine-D, L-sulfoximine (MSO)-induced seizures can be partially antagonized by pretreatment with 5FMOrn. However, the effect is considerably smaller than against ammonia-induced convulsions, although at the time of seizure onset brain ammonia levels of MSO-intoxicated mice were lower than in the animals receiving ammonium acetate. This suggests that MSO-convulsions are not entirely due to the elevation of brain ammonia concentrations, even though MSO administration mimics effects of ammonia on cortical inhibitory neuronal interactions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced endogenous ornithine concentrations protect against tonic seizures and coma in acute ammonia intoxication. 809 10


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