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

Regional cerebral blood flow (CBF) and regional cerebral glucose utilization (CGU) were studied by quantitative autoradiographic techniques in rats. Animals were treated either with a toxic dose of soman, an irreversible organophosphorus cholinesterase inhibitor, that produced convulsions or with saline as controls. An increased arterial blood pressure (mean increase = 41% of control) always preceded onset of convulsions. Convulsive activity was associated with an increase of plasma glucose concentration and marked increases over controls of CGU [average of all regions: control = 75 +/- 5 mumol.100 g-1.min-1, n = regions/animals (304/8); seizures = 451 +/- 20 mumol.100 g-1.min-1, n = 190/5] and CBF [average of all regions: control = 135 +/- 6 ml.100 g-1.min-1, n = 190/5; seizures = 619 +/- 29 ml.100 g-1.min-1, n = 190/5). Regional distribution of these effects revealed a greater proportional increase of CBF over CGU in cingulate, motor, and occipital cortex and caudate-putamen. In contrast, a lower proportional increase of CBF over CGU in CA3 region of hippocampus, dentate gyrus, medial thalamus, and substantia nigra was observed, implying the existence of a relative ischemia in these brain areas. These findings may be relevant to the pathogenesis of brain lesions associated with soman-induced convulsions.
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PMID:Cerebral blood flow and metabolism in soman-induced convulsions. 161 57

Glutamate (GLU)-receptor subtypes, (quisqualate (QA)-, kainate (KA)-, N- methyl-D-aspartate (NMDA)-receptors) and the phencyclidine sites localized in the ion-channel associated to the NMDA-receptors, were studied by autoradiography in the hippocampus of rats subjected to a convulsive dose of the acetylcholinesterase inhibitor soman (0-, 1,2,2-trimethylpropyl methylphosphonofluoridate). In intoxicated rats, a significant increase in L-[3H]-GLU binding occurred within the first 40 min of seizures in the hippocampal CA3 and CA1 areas. Whereas binding to KA- and NMDA-receptors remained unchanged, L-[3H]-GLU binding to CA3 QA-receptors increased by 31 and 50% respectively after 10 and 40 min of seizures. In CA1, the change in QA-receptors was delayed (+30% after 40 min) and accompanied by an increase in the phencyclidine site binding capacity, reflecting the probable concomitant opening of NMDA ion-channels. These findings confirmed the previously suspected involvement of GLU in the earliest stages of soman-induced seizures, and suggested that, in hippocampus, the primary activation of QA-receptors in the CA3 region could lead to the secondary recruitment of combined non-NMDA (QA) and NMDA mechanisms in CA1.
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PMID:Involvement of the different rat hippocampal glutamatergic receptors in development of seizures induced by soman: an autoradiographic study. 166 52

The levels of prostaglandin F1 (6-keto-PGF1 alpha), thromboxane B2 (11-dehydro-TxB2), and peptidoleukotriene C4 (LTC4) were measured (acetylcholinesterase immunoassay) in the frontal cortex (FC) and the striatum (SA) of the rat brain to study the possible role of eicosanoids in seizures induced by hyperbaric oxygen (HBO). The rats were exposed to (1) hyperbaric oxygen (HBO, 6 ATA O2) up to the first seizure (2) compressed air (6 ATA air, i.e., approximately equal to 1.25 ATA O2) or (3) atmospheric pressure (1 ATA air, i.e., 0.21 ATA O2); there was no seizure in groups 2 and 3. Transition from 6 ATA to atmospheric pressure was obtained in 15 min; the rats were then decapitated and their heads frozen in liquid nitrogen before extraction and analysis of prostanoids. Whatever the conditions, cortical levels of 6-keto-PGF1 alpha and 11-dehydro-Tx B2 are higher than striatal levels; considering the same area, 11-dehydro-Tx B2 and LTC4 concentrations were not significantly different whatever the condition, but there is a trend for lower 6-keto-PGF1 alpha levels in FC after HBO seizure. Biochemical mechanisms are discussed. Eicosanoids do not seem to play a major role in HBO seizures, although some modifications of their metabolism may take place.
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PMID:The influence of one hyperbaric oxygen-induced seizure on brain eicosanoid content. 177 30

Extracellular amino acid levels in CA3 and CA1 fields of rat hippocampus, an area highly sensitive to seizures, were determined by intracranial microdialysis during seizures induced by systemic administration of soman (o-1,2,2-trimethylpropyl methylphosphonofluoridate), a potent inhibitor of acetylcholinesterase. The glutamate uptake level was determined on another series of animals in hippocampus homogenates. An early and transient increase in the extracellular glutamate level occurred in CA3 within 30 min of seizures, with correlated brief elevations of taurine, glycine and glutamine levels. The glutamate level increased early in CA1, declined and then became more sustained (after 50 min of seizures). Apparent elevations of taurine, glycine and glutamine levels in CA1 accompanied changes in glutamate concentrations. Changes of glutamate level correlated with an increase in the glutamate uptake which rapidly declined after 40 min of seizures. The role of the transient release of glutamate in CA3 and of the sustained release in CA1 in prolonged soman-induced seizures is considered. The correlation between glutamate and other amino acid release is studied.
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PMID:Effects of soman-induced seizures on different extracellular amino acid levels and on glutamate uptake in rat hippocampus. 178 36

A 3-year-old boy developed confusion, generalized tonic-clonic seizures, and sustained ventricular tachycardia following ingestion of an unknown quantity of orphenadrine (Norflex). Although refractory to precordial thump, synchronous cardioversion, and lidocaine, the ventricular tachycardia was reversed by intravenous administration of the tertiary acetylcholinesterase inhibitor physostigmine. We discuss the underlying physiology and manifestations of anticholinergic overdose, the specific manifestations of orphenadrine overdose, and the current recommendations regarding the utilization and toxicity of physostigmine in the treatment of anticholinergic syndromes and orphenadrine intoxication.
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PMID:Reversal of orphenadrine-induced ventricular tachycardia with physostigmine. 844 95

During seizures induced by soman, an organophosphorus compound, irreversible inhibitor of acetylcholinesterase, the intra-amygdaloid microdialysis of extracellular glutamate, an excitatory amino-acid, showed a sustained increase, more rapid than in hippocampus. This result suggests an early involvement of the amygdala in the development of soman-induced seizures. Moreover, the ex vivo, study by quantitative autoradiography of the binding of tritiated TCP (thienyl-phencyclidine) does not reveal an opening of ionic channels linked to N-methyl-D-aspartate (NMDA) sensitive receptors of glutamate, during seizures, unlike in the hippocampus. This difference could indicate, according to other experimental models, that in amygdala the release of glutamate could occur massively without repeated stimuli as in the hippocampus.
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PMID:[Involvement of glutamatergic system of amygdala in generalized seizures induced by soman: comparison with the hippocampus]. 183 48

1. Chronic administration of the benzodiazepine inverse agonist FG 7142 has previously been shown to induce seizure activity in mice. In the present study we have investigated the effects of acute and chronic treatment with FG 7142 in mice on the levels of acetylcholinesterase activity in cortex, hippocampus, midbrain and striatum. We have also investigated the effects of acute and chronic stress in the form of handling (vehicle-injection) on acetylcholinesterase levels. 2. A single dose of FG 7142 produced a marked elevation of total acetylcholinesterase activities in the hippocampus and midbrain when compared with vehicle-injected control levels, but the levels were not different from those in unhandled animals. 3. Acute stress, in the form of vehicle-injection produced decreases in cortical and hippocampal soluble acetylcholinesterase activity but FG 7142 had no effect upon these stress-induced changes. 4. Total cortical and hippocampal acetylcholinesterase activities were increased by 56% and 16% respectively in the chronic FG 7142-treated mice that exhibited seizure activity (compared with vehicle-injected controls). 5. Soluble acetylcholinesterase activity in the midbrain was decreased to 82% of control levels only in animals that had undergone FG 7142-induced kindling. Smaller or no changes in acetylcholinesterase activity in the midbrain were observed in chronically FG 7142-treated animals that exhibited no seizure activity. 6. Mice that did not demonstrate seizure activity in response to chronic FG 7142 treatment showed alterations in the soluble acetylcholinesterase activities of the hippocampus and midbrain. 7. It is concluded that chronic treatment with the benzodiazepine inverse agonist FG 7142 produces alterations in the acetylcholinesterase activities of various brain regions, in a manner related to the kindling that can be produced by this treatment. 8. Chronic mild stress, in the form of repeated handling (vehicle injection), induced changes in brain activity with decreases in total activity occurring in the cortex and hippocampus, and an increase in soluble acetylcholinesterase activity occurring in the midbrain. 9. All these stress-induced changes appeared to be prevented by administration of FG 7142 at the time of the stress. It would appear therefore that FG 7142 can prevent the effects of chronic stress on brain acetylcholinesterase activity.
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PMID:Acetylcholinesterase activity in regions of mouse brain following acute and chronic treatment with a benzodiazepine inverse agonist. 196

In rats poisoned with soman (s.c. 100 micrograms/kg), a potent inhibitor of cholinesterase (ChE), the numbers of dendritic spines of Golgi impregnated hippocampal pyramidal cells (CA1 sector) were evaluated within the first hour of the intoxication. Animals that experienced convulsions showed a rapid and striking decrease in the density of dendritic spines which could be reduced by nearly 80% of the controls in the basal dendrites 60 min post-soman exposure. Although the exact mechanisms cannot be determined from the present study, it is suggested that the spine loss may represent: (1) the first sign of the seizure-related neuronal changes which are known to occur later during soman intoxication; and (2) the expression of the 'dendrotoxic' effects produced by certain non-cholinergic excitatory transmitters such as glutamate.
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PMID:Early dendritic changes in hippocampal pyramidal neurones (field CA1) of rats subjected to acute soman intoxication: a light microscopic study. 205 43

Soman, an organophosphorous irreversible inhibitor of acetylcholinesterase, was studied for its effect on the rat blood-brain barrier (BBB) during the first 24 h of intoxication. Young adult male Sprague-Dawley rats, injected with Evans blue-dye and surviving a subsequent single convulsive dose of soman (114 micrograms/kg, 0.9LD50), presented focal and diffuse penetration of dye in areas of brain normally considered protected by the BBB. Invasion was widest during the first hour when signs of excitation, respiratory distress and convulsions peaked and was absent at 24 h. During this time period, cholinesterase inhibition, as measured by enzyme assay, persisted in brain and blood at 10% and 6% of control values respectively. Brains of nonconvulsing animals and animals pretreated with nembutal (45 mg/kg, I.P.) or with diazepam (10 mg/kg, I.P.) were free of extravasated dye. A ranking of dye-breached brain areas suggested that cerebellar and cerebral cortex were most frequently involved while brain stem was rarely stained. Ultrastructural analysis of breached areas with horseradish peroxidase as a tracer molecule, revealed that the probable subcellular mechanism of the induced breach was enhanced vesicular transport, a mechanism similarly described for seizure. Consequences of the breach were emphasized with the detection of significantly elevated levels of an exogenously administered quaternary compound, 3H-hexamethonium. These findings present additional evidence that an anticholinesterase-induced breach of the rat blood-brain barrier is convulsive dependent, demonstrates BBB mechanisms similar to that of seizure, and can allow CNS penetration of blood-borne drugs and circulatory proteins that normally would be slowed or excluded by an intact BBB.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of an anticholinesterase compound on the ultrastructure and function of the rat blood-brain barrier: a review and experiment. 207 Mar 59

In our previous study, we have demonstrated that intra-amygdaloid injection of dibutyryl-cAMP causes neuronal damage in the injected AM and the CA 1-3 subfields of the ipsilateral hippocampus in addition to epileptic seizures. This result suggested that db-cAMP is a new neuroexcitotoxin. In this study, we examined comparative morphological effect on acetylcholinesterase (AChE) following intra-amygdaloid injection of db-cAMP or, kainate. In Expt. 1, twenty rats received 100 micrograms db-cAMP (N = 10), 0.5 micrograms kainate (N = 4), or saline as a vehicle (N = 6), through the implanted cannula under non-anesthesia. Either kainate or db-cAMP produced epileptic seizures, while saline induced no electroclinical ictal response. Following db-cAMP or kainate injection, neuronal loss was observed in the injected AM, but AChE positive fibers were intact. In the hippocampus ipsilateral to the injected AM, the loss of pyramidal cells was also noted in accordance with the severity of seizure intensity. In the piriform cortex ipsilateral to the injected AM, the loss of AChE-positive fibers were seen, but sparing neuronal cell bodies. In Expt. 2, nineteen rats were injected with 100 micrograms db-cAMP (N = 7), 0.5 micrograms kainate (N = 7), or saline as a vehicle (N = 5) under pentobarbital anesthesia. Kainate or db-cAMP produced few sporadic spikes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Neuroexcitotoxic action of db-cAMP: lesioning of neuronal cell bodies while sparing fibers of passage]. 216 8


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