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

Several previous studies have demonstrated increased synthesis of cerebral prostaglandins (PGs) following convulsive activity. In addition, it has been proposed that endogenous prostanoids have anticonvulsive properties and may act to attenuate or limit seizure activity in vivo. In this study we have used focal injections of prostaglandins (PGs) to examine their potential modulatory effects on electrically kindled seizure activity. We report that the intra-amygdaloid administration of PGD2, PGE2 or PGF2a, (1-10 micrograms) showed no significant effects on any of the kindled seizure parameters studied. The highest dose of PGF2a was ineffective at all pretreatment times between 2-30 mins. Our data is inconsistent with the view that PGs exert protective effects against seizure activity, at least within the amygdala against electrically kindled seizures.
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PMID:Lack of effect of focally administered prostaglandins on electrically kindled seizure activity. 177 Dec 37

Endogenous cerebral prostanoids possess anticonvulsant properties. This study investigates possible age-dependent anomalies of prostanoid synthesis in the brain of seizure-prone DBA/2J (DBA2) mice as compared to sound stimulus-resistant CFLP mice. Irrespective of the age of the animals, a large increase of prostaglandin (PG) D2 and E2 in the brain of CFLP mice was observed in response to pentylenetetrazol (PTZ)-, or electroshock (ES)-induced seizures. Significantly less PGD2 and PGE2 was formed in the brain of DBA2 mice at day 21 after birth when subjected to PTZ or ES convulsions. At 42 days of age, however, this deficit of cerebral PGD2 synthesis in DBA2 mice disappeared concomitantly with the age-related decrease in audiogenic seizure (AS) susceptibility, whereas the deficit of PGE2 formation persisted. These results suggest that a deficiency of cerebral PGD2 synthesis may be one of the factors responsible for the AS susceptibility of the DBA2 mice. In contrast to PTZ or ES convulsions, acoustically induced seizures of the DBA2 mice were not accompanied by cerebral prostanoid synthesis. This supports the view that the pathways involved in AS are different from those involved in PTZ or ES models of epilepsy.
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PMID:Differential prostaglandin formation induced by convulsions in the brain of mice susceptible (DBA/2J) and resistant (CFLP) to acoustic stimulation. 232 14

Electrically- and chemically-induced convulsions, as well as spontaneous convulsions, triggered off a large increase in brain PG synthesis occurring mainly in cerebral cortex and hippocampus. Prevention of PG synthesis by cyclooxygenase inhibitors had no influence on the onset of the first clonic seizure, but markedly reduced the latency time of the final tonic seizure. Accordingly, also the acute toxicity of the convulsant PTZ was enhanced after cyclooxygenase inhibition by various NSAIDs (decrease in LD50). On the other hand, if brain concentrations of prostanoids were increased by a preceding ECS treatment, the onset of PTZ-induced clonic seizures was markedly delayed, and the acute toxicity of the convulsant was reduced. Both effects were abolished after inhibition of PG synthesis. The major cerebral PG formed during convulsions (PGD2) proved to have anticonvulsive properties when injected i.c.v. Also, in convulsion-prone gerbils, anticonvulsive effects of cerebral PGs were observed. These results suggest that endogenously formed brain PGs possess anticonvulsive properties of biological relevance.
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PMID:Formation and functions of prostaglandins in the central nervous system in rodents. 293 71

Basal levels of 5 cerebral prostanoids (PGD2, PGF2 alpha, PGE2, 6-keto-PGF1 alpha and thromboxane/TX/B2) were measured radioimmunologically in normal and convulsion-prone gerbils. Significantly less PGD2,PGE2 and 6-keto-PGF1 alpha was found in the brain of seizure-sensitive animals. After treatment with indomethacin, which reduced the amount of brain cyclo-oxygenase products, also normal gerbils exhibited convulsions following environmental stress. The results are in accordance with the hypothesis that endogenous prostanoids play a role in the regulation of seizure susceptibility.
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PMID:Decreased levels of brain cyclo-oxygenase products as a possible cause of increased seizure susceptibility in convulsion-prone gerbils. 643 Apr 71

Seizures were induced in a strain of epileptic gerbils by moderate environmental stress. Concentrations of five different cyclooxygenase products (PGD2, PGF2 alpha, PGE2, 6-keto-PGF1 alpha and thromboxane B2) were measured in brain by specific radioimmunoassays before and at different time intervals after the onset of clonic-tonic convulsions. All prostanoids markedly increased subsequent to the convulsions. Maximal concentrations were reached after about 15 min. The major compound detected was PGD2, followed by PGF2 alpha and lower concentrations of the other cyclooxygenase products. Indomethacin completely prevented the convulsion-induced formation of prostanoids. Fifteen min after a first seizure almost all animals proved to be protected against a second convulsion. Indomethacin pretreatment markedly reduced the number of convulsion-resistant animals. These findings are compatible with the hypothesis that endogenous prostaglandins exert anticonvulsive effects.
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PMID:Anticonvulsive effects of endogenous prostaglandins formed in brain of spontaneously convulsing gerbils. 643 84

Seizures were induced in female Wistar rats by electroconvulsive shock (ECS) or administration of pentetrazole (PTZ). Brain content of various prostanoids measured by radioimmunoassay showed time-dependent changes after the induction of convulsions; highest levels were found for PGD2 followed by PGF2 alpha, PGE2, TXB2 and 6-keto-PGF1 alpha. Analysis of the various arachidonic acid metabolites in seven parts of the rat brain dissected according to the method of Glowinski and Iversen revealed the largest increases in hippocampus and cerebral cortex and smaller ones also in hypothalamus and corpus striatum both after ECS and PTZ. The ratios of the different cyclo-oxygenase products remained virtually the same in whole brain as well as in those regions where the formation of prostaglandins was markedly elevated. 15-keto-13,14-dihydro-PGF2 alpha also increased simultaneously in parallel to its parent compound, PGF2 alpha and was detected in significant amounts only in hippocampus and cerebral cortex. However, concentrations of 15-keto-13,14-dihydro-PGF2 alpha in these brain regions as well as in whole brain represented only 3-10% of the amounts found for PGF2 alpha. Thus, the metabolizing enzymes 15-hydroxy-PG-dehydrogenase and delta 13-PG-reductase seem to be of minor importance for the inactivation of prostanoids in brain tissue.
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PMID:Regional distribution of arachidonic acid metabolites in rat brain following convulsive stimuli. 679

The levels of 5 different prostanoids (PGD2, PGF2 alpha, PGE2, TXB2 and 6-keto-PGF1 alpha) formed in whole mouse brain in vivo were measured by specific radioimmunoassays. Basal concentrations were found to be very low (few ng/g wet weight). A marKed increase occurred during convulsions induced by either pentylenetetrazole or by electroconvulsive shock. Under both conditions the major cyclooxygenase product detected was PGD2, followed by PGF2 alpha and lower concentrations of the other prostanoids. The non-steroidal anti-inflammatory drugs flurbiprofen, indomethacin, and diclofenac dose-dependently inhibited the pentylenetetrazole-induced formation of prostaglandins. Concomitantly these 3 compounds dose-dependently increased the acute toxicity of pentylenetetrazole (decrease in LD50). Conversely, if levels of cerebral prostaglandins were enhanced by a preceding electroshock, the toxicity of pentylenetetrazole was significantly reduced (increase in LD50), and the time of onset of clonic seizures was markedly prolonged. Both the effect on the latency time and the LD50 could be reversed if the cerebral prostaglandin synthesis was prevented by indomethacin, or if the time interval between the electroshock and pentylenetetrazole administration was extended, so that the electroshock-stimulated prostaglandin concentrations had declined to basal levels again. These findings indicate that endogenous prostanoids formed in mouse brain during convulsions might possess anticonvulsive properties.
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PMID:Potential anticonvulsive properties of endogenous prostaglandins formed in mouse brain. 680 23

This study was undertaken to evaluate the role of brain PGD2 activity during PTZ induced seizures in rats. Potentiation of endogenous PGD2 activity caused an anti-convulsant effect. Thus, after PGD2 injection (5 microg/icv) the latency of generalized tonic clonic convulsions was prolonged. ZK 118.182, a stable analogue of PGD2, dose-dependently inhibited the incidence and the intensity of seizures when injected at doses of 1-100 ng/icv. But on the other hand, inhibition of PGD2 activity either by a D-type PG receptor antagonist (AH 6809; 50 ng/icv) or by a PGD synthase inhibitor (sodium selenite; 0.2 microg/icv) produced a proconvulsant effect by increasing the incidence and the intensity of the seizures. These findings indicate that endogenous PGD2 activity in the brain may have a specific inhibitory role for the initiation and propagation of PTZ induced seizures in rats.
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PMID:Inhibition of pentylenetetrazol-induced seizures in rats by prostaglandin D2. 955 45

In the brain, S100 protein and neuron-specific enolase (NSE) are mainly found in glial cells and neurons, respectively. We investigated concentrations of S100 protein and NSE in cisternal cerebrospinal fluid obtained during implantation of foramen ovale electrodes in eight patients with temporal lobe epilepsy (TLE). In addition, the meningeal markers cystatin-C and beta-trace as well as total protein were measured. Patients with trigeminal neuralgia (TN) undergoing glycerol rhizotomy served as controls. S100 protein and NSE levels ipsilateral to the site of seizure onset were significantly higher than in TN. Contralateral TLE values were also markedly but not significantly elevated. The meningeal markers cystatin-C and beta-trace protein as well as total protein did not differ in TLE and TN. We conclude that interictal temporal lobe dysfunction corresponds with neuronal and glial marker elevations in the extracellular space and that site-specific elevations may predict the site of seizure origin biochemically.
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PMID:Cisternal S100 protein and neuron-specific enolase are elevated and site-specific markers in intractable temporal lobe epilepsy. 1046 53

Congenital disorders of glycosylation (CDG), formerly known as carbohydrate-deficient glycoprotein syndromes, lead to diseases with variable clinical pictures. We report the delineation of a novel type of CDG identified in 2 children presenting with severe developmental delay, seizures, and dysmorphic features. We detected hypoglycosylation on serum transferrin and cerebrospinal fluid beta-trace protein. Lipid-linked oligosaccharides in the endoplasmic reticulum of patient fibroblasts showed an accumulation of the dolichyl pyrophosphate Man(5)GlcNAc(2) structure, compatible with the reduced dolichol-phosphate-mannose synthase (DolP-Man synthase) activity detected in these patients. Accordingly, 2 mutant alleles of the DolP-Man synthase DPM1 gene, 1 with a 274C>G transversion, the other with a 628delC deletion, were detected in both siblings. Complementation analysis using DPM1-null murine Thy1-deficient cells confirmed the detrimental effect of both mutations on the enzymatic activity. Furthermore, mannose supplementation failed to improve the glycosylation status of DPM1-deficient fibroblast cells, thus precluding a possible therapeutic application of mannose in the patients. Because DPM1 deficiency, like other subtypes of CDG-I, impairs the assembly of N-glycans, this novel glycosylation defect was named CDG-Ie.
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PMID:Deficiency of dolichol-phosphate-mannose synthase-1 causes congenital disorder of glycosylation type Ie. 1064 90


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