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

The influence of electrical and chemical stimulation of nucleus caudatus (NC) on bioelectrical seizure activity of amygdala (Am) was studied in rabbits. The electrical stimulation of NC inhibits seizures in Am induced by the administration of picrotoxin into this nucleus. Dopamine (DA) and cholinomimetics-metacholine and neostygmine-applied into NC inhibit seizures in Am. Noradrenaline (NA) acts biphasically, first potentiating and then inhibiting seizures in Am. Serotonin (5-HT) and glutamic acid (GA) administered to NC do not affect the seizures. In the case of seizures excited by electrical stimulation, DA and neostygmine possessed inhibiting action; NA, too, inhibited seizures without, however, inducing primary stimulation. Similarly as in the case of picrotoxin-stimulated seizures, neither 5-HT nor GA brought about the effects. The present study deals with the correlation of dopaminergic anc cholinergic systems in NC.
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PMID:The influence of neuromediators injected into nucleus caudatus on bioelectrical seizure activity of amygdala. 0 50

A Canadian Indian family is described in which three of the children were mentally retarded, and had seizures and other neurological abnormalities. They had chronic metabolic acidosis associated with elevated blood levels of lactate, pyruvate, and alanine. Two of the children excreted large amounts of pyruvic and alpha-ketoglutaric acids in the urine and had elevated plasma levels of glutamic acid and proline. Hypoglycemia occurred with fasting in two of the children. Treatment with pharmacological doses of thiamine, lipoic acid, biotin, riboflavin, and various dietary regimes was without effect. One child died at 3 1/2 months and another at 4 1/2 months; the third is still alive at 23 months of age. Enzyme assays revealed a low level of activity of both the pyruvate and alpha-ketoglutarate dehydrogenase complexes in cultured fibroblasts of one of the sibs. These patients appeared to have partial defects in the oxidation of pyruvate, as well as of alpha-ketoglutarate within the tricarboxylic acid cycle.
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PMID:Lactic acidosis in three sibs due to defects in both pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes. 18 26

A 13 1/2-year-old child died with vitamin B6-dependent seizures in progress. Microscopic findings in brain included an abnormally sparse quantity of central myelinated fibers in the cerebral hemispheres. Glutamic acid concentrations were elevated and GABA concentrations reduced in the frontal and occipital cortices but not in the spinal cord. All other amino acid concentrations were normal, except for increased cystathionine in the occipital cortex. Pyridoxal-5-phosphate (PLP) was reduced in the frontal cortex. Glutamic acid decarboxylase activity comparable to that of controls was detected when the PLP concentration was greater than 0.05 mM. These findings suggest that pyridoxine-dependent seizures in man are associated with reduced GABA concentrations in the brain and with diminished central white matter structures.
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PMID:Vitamin B6-dependent seizures: pathology and chemical findings in brain. 56 38

Susceptibility to audiogenic seizures can be induced in some strains of resistant mice by exposure to an initial auditory stimulus (acoustic priming). Aminooxyacetic acid, hydrazine, glutamic acid, gamma-aminobutyric acid (GABA), cycloheximide, and metyrapone antagonize the acoustic priming of audiogenic seizure susceptibility in C57BL/6Bg mice, whereas only metyrapone attenuates that of DBA/1Bg-asr mice. The strain difference in the effect of AOAA and cycloheximide is correlated with a small, transient fall in level of brain GABA in C57BL/6Bg but not DBA41Bg-asr mice. These findings support our hypothesis that there are at least two neural mechanisms of acoustic priming, each with its own genetic basis and that corticosteroids are required by both mechanisms for the development of primed seizures.
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PMID:Pharmacogenetic differences in audiogenic seizure priming of C57BL/6Bg and DBA/1Bg-asr mice. 92 78

A significant increase in the plasma levels of glutamic acid and a significant decrease in aspartic acid and taurine in epileptic patients and their first degree relatives was reported more than a decade ago and an underlying genetic basis for these amino acid changes was suggested. The main objective of the present study was to determine the plasma levels of glutamic acid, aspartic acid and taurine in El mice which are an inbred epileptic mutant mouse strain. The results show a significant increase in plasma glutamic acid but no changes in aspartic acid or taurine in the epileptic mice as compared to controls. The data provide the first evidence of a significant increase in plasma glutamic acid in an animal model of hereditary epilepsy and substantiate the hypothesis that a genetic defect underlies the elevated plasma glutamic acid levels in association with epilepsy. The findings are also compatible with neurochemical and neurophysiological evidence implicating glutamic acid in the mechanism of seizures.
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PMID:Increased plasma glutamic acid in a genetic model of epilepsy. 135 88

The effects of three dipeptide analogues of N-acetylaspartylglutamate on seizures elicited by intracerebroventricular (i.c.v.) injection of L-glutamate (GLU), N-methyl-D-aspartate (NMDA), kainate (KA) and intraperitoneal (i.p.) injection of pentylentetrazol (PTZ) were studied in mice. N-Ac-L-Phe-L-Glu was active against myoclonic seizures induced by GLU and NMDA under simultaneous i.c.v. injection. All dipeptides were ineffective against KA and PTZ convulsions. The anticonvulsant activity and potency of N-Ac-L-Phe-L-Glu were similar to that of gamma-D-glutamylglycine (gamma-DGG) for excitatory amino acids (EAA) induced seizures. These results indicate EAA antagonistic activity among dipeptides which have L-glutamic acid on C-terminal and acetylated N-terminal.
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PMID:Dipeptides--analogues of N-acetylaspartylglutamate inhibit convulsive effects of excitatory amino acids in mice. 167 19

The amino acids L-glutamic and L-aspartic acids form the most widespread excitatory transmitter network in mammalian brain. The excitation produced by L-glutamic acid is important in the early development of the nervous system, synaptic plasticity and memory formation, seizures and neuronal degeneration. The receptors activated by L-glutamic acid are a target for therapeutic intervention in neurodegenerative diseases, brain ischaemia and epilepsy. There are two types of receptors for the excitatory amino acids, those that lead to the opening of cation-selective channels and those that activate phospholipase C (ref. 11). The receptors activating ion channels are NMDA (N-methyl-D-aspartate) and kainate/AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate)-sensitive receptors. The complementary DNAs for the kainate/AMPA receptor and for the metabotropic receptor have been cloned. We report here on the isolation and characterization of a protein complex of four major proteins that represents an intact complex of the NMDA receptor ion channel and on the cloning of the cDNA for one of the subunits of this receptor complex, the glutamate-binding protein.
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PMID:Cloning of cDNA for the glutamate-binding subunit of an NMDA receptor complex. 183 48

This study extends our previous work in which we described the presence of an interictal behavioral disturbance in a chronic animal model of temporal lobe epilepsy (TLE). In this study, we investigated the cerebrospinal fluid (CSF) neurotransmitter changes underlying the development of chronic recurrent seizures of temporal lobe origin and interictal behavioral disturbance in cats made epileptic after intrahippocampal injection of kainic acid (KA). Using high-performance liquid chromatography, we measured 22 putative neurotransmitter amino acids. After intrahippocampal KA injection, cats developed an initial acute period of intense seizure activity. Cisternal CSF amino acids, which were repeatedly sampled during the acute period through a permanent indwelling cannula, were unchanged apart from a mild elevation in CSF alanine. The high-level seizure activity gradually decreased, and cats entered a chronic epileptic period characterized by recurrent yet intermittent temporal lobe seizures. CSF GABA levels during the chronic epileptic period were significantly decreased. In contrast, CSF levels of other amino acids--alanine, tyrosine, taurine, aspartic acid, and glutamic acid--did not change significantly. Behavioral testing also showed a heightened interictal defensive reactivity during the chronic epileptic period. To the extent that CSF GABA concentration reflects brain GABA concentration, this study suggests that a decrease in brain GABA may contribute both to the epilepsy and interictal emotional lability of animals with a chronic seizure disorder of temporal lobe origin.
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PMID:Interictal behavioral alterations and cerebrospinal fluid amino acid changes in a chronic seizure model of temporal lobe epilepsy. 174 47

Sudden cooling of the isolated spinal cord of frogs results in characteristic seizure-like activity in the hind legs. In the present investigation, these spinal seizures induced by sudden cooling (SSSC) were studied to determine whether excitatory amino acids (EAAs) are involved in the mediation of this activity. The nonspecific EAA antagonist, L-glutamic acid diethyl ester and cis-2,3-piperidine dicarboxylic acid inhibited the clonic and tonic phase of SSSC after intralymphatic or intrathecal administration. The antagonist gamma-D-glutamylaminomethylsulfonic acid and gamma-D-glutamyltaurine also suppressed both phases after intrathecal injections. The NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid, DL-2-amino-7-phosphonoheptanoic acid, and 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid were effective inhibitors of the tonic phase and actually prolonged the duration of the clonic phase, an effect similar to that observed after low doses of gamma-D-glutamylglycine. SSSC were resistant to spinal perfusion to tetrodotoxin (1 microM). The concentrations of glutamate, aspartate, and glycine were increased in the Ringer's solution surrounding rapidly cooled spinal cord slices, but only in cords from species that elicited some magnitude of SSSC, not in cords from species resistant to induction of SSSC. Our data support the hypothesis that EAAs play a role in SSSC via activation of quisqualate receptors.
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PMID:Spinal seizures evoked by sudden cooling of amphibian isolated spinal cords: involvement of excitatory amino acids. 183 Aug 37

Rats were kindled to two consecutive class 5 seizures by once-daily entorhinal electrical stimulation. After one stimulus-free month, in vitro Ca2(+)-dependent, K(+)-stimulated endogenous amino acid release was measured in regio superior, regio inferior and dentate gyrus of the hippocampal formation. Ca2(+)-dependent L-glutamate release was robust in all 3 regions of controls and greatest in dentate gyrus; release of GABA and L-aspartate were significant in regio superior and dentate gyrus. L-Glutamate release was significantly enhanced in ipsilateral regio inferior of kindled hippocampus and tended to be greater contralaterally. This pattern was not seen in regio superior or dentate gyrus. These studies, in concert with others, suggest that Ca2(+)-dependent L-glutamate release in hippocampus is augmented by entorhinal kindling and that this enhanced release may be primarily from presynaptic granule cell mossy fiber projections.
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PMID:Entorhinal kindling permanently enhances Ca2(+)-dependent L-glutamate release in regio inferior of rat hippocampus. 196 56


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