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

Electrographic and behavioral seizures were induced in rats by repeated electrical stimulation of the dorsal hippocampus for three consecutive days. Animals were killed in the following groups: Control group; group killed during the clonus phase of a convulsion in the third stimulating session; group killed 10 minutes after the termination of a convulsion in the third stimulating session. Membrane ATPase activity was shown to be significantly increased in the group killed during the clonic phase compared to that of the control group and was significantly reduced post-convulsively, compared to both the control group and the group killed during the convulsion. The results suggest a modification of enzyme activity which may be important in the initiation and maintenance of seizure activity.
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PMID:Epilepsy and membrane Na+K+ATPase: changes in activity using an experimental model of epilepsy. 610 Sep 44

This study describes the preliminary isolation of substances from beef brain cortex which are required to produce an oxygen-induced enhancing effect on Na, K-ATPase. Evidence is presented that at least 3 fractions--a heat stable, low molecular weight proteinaceous substance, a cholesterol rich, membranous component, and an as yet unidentified substance--are required to produce oxygen enhancement of Na, K-ATPase activity. These findings have specific ramifications in neurocellular physiology, especially as related to seizures.
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PMID:Enhancement of cortical Na+,K+-ATPase by increased oxygen tensions: evidence of a new controlling mechanism. 612 51

DBA/2J mice are susceptible to audiogenic seizures (ASs) in an age-dependent manner, susceptibility being maximal at 21 days of age and declining thereafter. DBA, as compared with AS-resistant C57BL/6J (C57) mice, had higher carbonic anhydrase (CA) activity in cerebral cortex, brainstem, and cerebellum homogenates at 21 days of age. CA activity was also increased in cytosolic (82%), microsomal (167%), and myelin (68%) subcellular fractions from cerebral cortex, and in cytosolic (51%) and mitochondrial (102%) fractions from brainstem of DBA mice at 21 days of age. In addition, DBA mice had a higher Na+, K+-ATPase activity in myelin from cerebral cortex, and a lower HCO3--ATPase activity in mitochondria from brainstem. The differences in CA activity in the cerebral cortex and in HCO3--ATPase were not present at 110 days of age, when DBA mice are no longer susceptible to ASs. Because CA and HCO3--ATPase are involved in maintaining a proper ionic environment for neuronal function, these data suggest that alterations in activity of these enzymes are related to the age-dependent changes in AS susceptibility in DBA mice.
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PMID:Subcellular distribution of carbonic anhydrase and Na+, K+- and HCO3--ATPases in brains of DBA and C57 mice. 623 73

Penicillin application to the rat brain motor cortex resulted in appearance of interictal discharges and seizures. After diazepam injection (2 mg/kg) a 100% increase in Na, K-ATPase activity of neuronal membranes in the epileptogenic focus was shown as compared to enzyme activity before diazepam injection. Interictal discharges and seizures changed in different ways after intramuscular injection of diazepam. The frequency and amplitude variation of interictal discharges increased but the seizures were suppressed. These effects increased with the dose of diazepam. It is suggested that the different influence of diazepam upon seizures and interictal discharges may reflect different mechanisms of these phenomena.
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PMID:[Electrical activity and Na, K-ATPase levels in an epileptic focus caused by application of penicillin to rat cerebral cortex and the effect of diazepam on them]. 625 82

Intraventricular (IVT) administration of digoxin (7.5 micrograms) induced 'popcorn-type' convulsions in rats. Though the convulsions looked similar to morphine-induced seizures, naloxone failed to antagonize these effects. Other anticonvulsants like phenobarbitone, ethosuximide, or GABAergic substances like piracetam and semicarbazide also had no protective effect against digoxin-induced convulsions. While calcium chloride potentiated these effects of digoxin, phenytoin, magnesium chloride, and potassium chloride treatment showed blocking actions. These observations suggest the involvement of Na/K-ATPase system in digoxin-induced convulsions. Clonidine and diazepam also provided protection against digoxin-induced convulsions through an unknown mechanism.
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PMID:Possible mechanism of digoxin-induced convulsions. 640 41

Na+,K(+)-ATPase (the sodium pump) is a ubiquitous enzyme that consumes ATP to maintain an adequate neuronal transmembrane electrical potential necessary for brain function and to dissipate ionic transients. Reductions in sodium pump function augment the sensitivity of neurons to glutamate, increasing excitability and neuronal damage in vitro. Temporal lobe epilepsy (TLE) is one disease characterized by hyperexcitability and marked hippocampal neuronal losses that could depend in part, on impaired sodium pump capacity secondary to changes in sodium pump levels and/or insufficient ATP supply. To assess whether abnormalities in the sodium pump occur in this disease, we used [3H]ouabain to determine the density of Na+,K(+)-ATPase for each anatomic region of hippocampus by in vitro autoradiography. Tissues were surgically obtained from epileptic patients with hippocampal sclerosis and compared with specimens from patients with seizures originating from temporal lobe tumors and autopsy controls. Changes in cellular population arising from neuronal losses or gliosis were assessed by protein densities derived from quantitative computerized densitometry of Coomassie-stained tissue sections. We estimated regional differences in capacity for ATP generation by determining cytochrome c oxidase (CO) activity. Principal neurons of hippocampus exhibit high levels of sodium pump enzyme. Both epilepsy groups exhibited slight but significant increases in sodium pump density/unit mass of protein in the dentate molecular layer, CA2, and subiculum as compared with autopsy controls. Greater hilar sodium pump density was also observed in sclerotic hippocampi. In contrast, CO activity was reduced in both epilepsy types throughout hippocampus. Results suggest that although sodium pump protein in surviving neurons appears to be upregulated in epilepsy, sodium pump capacity may be limited by the reduced levels of CO activity. Functional reduction in sodium pump capacity may be an important factor in hyperexcitability and neuronal death.
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PMID:Regional distributions of hippocampal Na+,K(+)-ATPase, cytochrome oxidase, and total protein in temporal lobe epilepsy. 760 16

We demonstrate that the enzyme family responsible for the restoration of the transmembrane cation balance, namely the sodium pump (Na+, K(+)-ATPase), plays a critical role in whether glutamate injures adult neurons in vivo. Partial inhibition of the sodium pump by the cardiac glycoside ouabain in young adult rats is not itself damaging. This treatment, however, markedly potentiates ordinarily subtoxic dosages of the glutamate analog kainic acid to produce limbic seizures and widespread neurodegeneration within the hippocampus in a pattern closely resembling that observed for human temporal lobe epilepsy.
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PMID:The cardiac glycoside ouabain potentiates excitotoxic injury of adult neurons in rat hippocampus. 764 34

Many neurological disorders are accompanied by abnormal nerve activity. However, the exact causes of this abnormal nervous activity has never been determined. Based upon my research, I propose a theory that the underlying cause of many types of neurological disorders such as minor epilepsy and narcolepsy is an abnormally functioning Na+/K+ ATPase pump at the molecular framework of the brain, notably the brainstem reticular formation (locus coerulus) and cerebellum in this particular case. The excessive and repetitive nerve activity within localized areas of the brain caused by abnormally functioning molecular Na+/K+ ATPase ion pumps may be the primary and true causes of many different types of neurological disorders since constant depolarizations of the cell membrane causes abnormally excessive amounts of certain neurotransmitters to be released. The type of neurological disorder may be a function of the abnormally occurring Na+/K+ ATPase molecular ion pump's localization within the neurological framework of the brain. To focus on my theory of repetitive nervous activity from abnormal inhibitive or defective Na+/K+ ATPase pumps, I have chosen to analyze minor epilepsy and narcolepsy intentionally. What is found is that the abnormal release of neurotransmitters during epileptic seizures or narcoleptic sleep episodes is secondary to the abnormal neuronal systematic framework underlying Na+/K+ membrane potentials since an abnormally inhibited or defective Na+/K+ ATPase pump has a direct electrogenic effect on the membrane potential.
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PMID:Abnormal cortical unit activity of the reticular formation. 785 71

A Ca(2+)- or Mg(2+)-stimulated ecto-ATPase is thought to regulate the hydrolysis of extracellular ATP in nervous tissues. The hydrolysis of nucleotide triphosphates (NTPs) was analyzed in brain microsomal fractions from crosses of DBA/2J (D2) and C57BL/6J (B6) mice. The nucleotide triphosphatase (NTPase) activity was significantly reduced in D2 mice as compared to B6 mice, and B6D2F1 hybrids had activities intermediate to the parentals. A significant positive correlation was found between the hydrolysis of four NTPs (ATP, CTP, GTP and UTP) in 24 B6 x D2 (BXD) recombinant inbred (RI) strains of mice and in 80 B6D2F1 x D2 backcross mice. The RI strains and backcross mice fell into two distinct groups with respect to the NTPase activity. Linkage of NTPase activity was suggested with the chromosome 2 markers, D2Mit6 and Ass-1, in the RI strains, and was confirmed by analysis of other markers in the backcross population. These data suggest that the Ca(2+)- or Mg(2+)-stimulated hydrolysis of NTPs, designated Ntp, is regulated by a single gene located on proximal chromosome 2. Although an association was observed previously between Ca(2+)-ATPase activity and susceptibility to audiogenic seizures (AGS), no significant association was observed for the expression of Ntp and AGS susceptibility.
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PMID:Genetic analysis of nucleotide triphosphatase activity in the mouse brain. 805 15

Transient changes in extracellular potassium concentration ([K+]o) and field potentials were evoked by 4-aminopyridine (4-AP; 50-100 microM) and recorded with ion-selective microelectrodes in CA1b, CA3b and dentate sectors of adult rat hippocampal slices. Long-lasting field potentials recurred at a frequency of approximately 1/60 s (0.016 +/- 0.003 Hz) in association with increases in [K+]o which were largest and most sustained in the dendritic regions where afferent fibers terminate (dentate > CA1 > CA3) and in the hilus. In stratum radiatum of CA1 or stratum moleculare of the dentate these fields had a peak amplitude of 1.4 +/- 0.29 mV, duration 8.3 +/- 1.6 s, and were accompanied by increases in [K+]o of 1.8 +/- 0.22 mM that lasted 32 +/- 5.5 s (n = 17 slices). Interictal epilentiform potentials, which were brief (< 0.2 s) and more frequent at approximately 1/3 s (0.30 +/- 0.02Hz) were also present in CA1, CA3 and the hilus and associated with small increases in [K+]o (< or = 0.5 mM, duration < or = 2 s). Interictal activity was blocked by 6-cyano-7-nitroquinoxalone-2,3-dione (CNQX; 5-20 microM); the slow, less frequent potentials were resistant to both CNQX and DL-2-amino-5-phosphonovaleric acid (APV; 50 microM) and reversibly blocked (or attenuated by approximately 80%) by bicuculline methiodide (BMI) (25-100 microM). The BMI-sensitive potentials were also abolished by baclofen (100 microM), an effect which was reversed by 2-OH-saclofen (100 microM). Focal application of KCI or GABA in the absence of 4-AP evoked long-lasting field and [K+]o potentials which were similar to those evoked by 4-AP but more sustained. The proportional relationship between the amplitudes of field and K+ potentials with GABA closely resembled that observed for 4-AP; in contrast the slope of KC1-evoked responses was lower. Our results demonstrate that in the adult rat hippocampus 4-AP induces in many different regions accumulations of [K+]o in synchrony with the long-lasting field potentials, which are known to correspond to an intracellular long-lasting depolarization of the pyramidal cells. These changes are smaller than those which occur in the immature rat hippocampus--which may be related to differences in Na-K-ATPase and susceptibility to seizures. These events involve the activation of GABAA receptors, are under the modulatory control of GABAB receptors, and likely arise from the activity of GABAergic interneuron and/or afferent terminals. The long-lasting field potentials appear to reflect mainly the direct depolarizing actions of GABA and to much more limited extent the associated accumulation of [K+]o.
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PMID:Extracellular K+ accumulations and synchronous GABA-mediated potentials evoked by 4-aminopyridine in the adult rat hippocampus. 874 Feb 10


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