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

Electrographic and clinical observations were made as long as 2 months after the injection of ibotenic acid (IBO) solution (50 micrograms in 1 microliter of phosphate buffer solution) through a chronically implanted cannula into unilateral amygdala of freely moving and non-anesthetized cats. The control group (phosphate buffer group) showed no change during the observation period. About 30 to 60 minutes after the injection of IBO, focal amygdaloid seizures occurred and propagated to the adjacent limbic structures. Clinically, attention and ipsilateral mydriasis were observed. The seizures occurred only 2 to 5 times and ceased within 4 hours. Cats became electroclinically normal afterwards. Histopathological examination revealed a small necrosis at the injected site of the amygdala. Remarkable pyknosis and gliosis were noted around the necrosis. Remote lesions such as neuronal cell loss and pyknosis were observed in the ipsilateral pyramidal cell layer of the hippocampus. But these changes were mild and not so severe as compared to our previous report of kainic acid microinjection in cats. Authors emphasized that IBO should be an excellent tool for lesion making and also suggested that an aseptic manipulation was essential in the lesion study in cats.
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PMID:[Ibotenic acid-induced limbic seizures and neuronal degeneration]. 362 Feb 20

Hydrolysis of membrane phospholipid phosphoinositides following ibotenate stimulation of an excitatory amino acid receptor subtype has recently been demonstrated to be a receptor-mediated biochemical response. The present study examined ibotenate-stimulated phosphoinositides hydrolysis, determined as accumulation of [3H]inositol 1-phosphate, in amygdala/pyriform cortical and hippocampal slices of amygdala-kindled rats which exhibited fully developed kindled seizures on 20 consecutive days. Animals which underwent a sham operation were used as controls. Ibotenate (10(-3) M)-stimulated accumulation of [3H]inositol 1-phosphate increased significantly by 191% in the amygdala/pyriform cortex (P less than 0.01) and by 59% in the hippocampus (P less than 0.05) of the amygdala-kindled rats killed 24 h after the last seizure. One week after the last seizure, a similar magnitude of significant increase (by 171%, P less than 0.05) was maintained in the amygdala/pyriform cortex of the amygdala-kindled rats. In contrast, the increase in the hippocampus had attenuated by this time, although accumulation of [3H]inositol 1-phosphate increased significantly (P less than 0.05) when stimulated by 10(-4) M ibotenate. These results suggest that enhancement of ibotenate-stimulated phosphoinositides hydrolysis in the amygdala/pyriform cortex may be associated with the long-lasting seizure susceptibility of amygdala-kindled rats.
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PMID:Increase in ibotenate-stimulated phosphatidylinositol hydrolysis in slices of the amygdala/pyriform cortex and hippocampus of rat by amygdala kindling. 367 28

Modeling studies revealed that progesterone, testosterone, and estradiol are stereochemically complementary to the cavity formed between base pairs in the DNA sequence, 5'-dTdG-3' X 5'-dCdA-3'. Each steroid aligned precisely with the topography of the cavity and formed 2 stereospecific hydrogen bonds linking phosphate oxygens on adjacent DNA strands. Hydrogen bonding donor-acceptor relationships were different for each hormone. The remarkable stereochemical specificity of the hormone-DNA complexes was demonstrated by the lack of complementarity of steroid enantiomers and steroid analogs having alternate ring systems and/or changes in the position of functional groups. Fit of molecules into DNA in the manner of the parent hormone correlated with biological activity. Antagonists also fit into the cavity but differed from agonists in their hydrogen bonding linkages to DNA and/or extended out of the cavity beyond the helix. Unlike flat intercalating agents which form stable complexes with DNA, wedge shaped steroids may thus be capable of forming reversible sequence-specific complexes with DNA. We conclude that the stereochemistry of DNA can be used to predict hormonal activity.
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PMID:The stereochemical complementarity of DNA and reproductive steroid hormones correlates with biological activity. 375 4

In vivo phosphorus 31 nuclear magnetic resonance (31P NMR) spectroscopy was used to evaluate changes in cerebral high-energy phosphate compounds in 8 infants with seizures. During the study 4 babies had seizures that caused a 50% decrease in the phosphocreatine to inorganic phosphate (PCr/Pi) ratio. Focal seizures caused lateralized decreases in the PCr/Pi ratio; generalized seizures caused bilateral decreases. Postictal spectra had increased PCr/Pi ratios, presumably due to postictal inhibition. Interictal 31P NMR spectra were normal. One patient's seizures were successfully treated with intravenously administered phenobarbital during NMR data acquisition, causing an immediate increase in the PCr/Pi ratio from 0.7 to 1.2. These studies indicate that cerebral PCr concentration decreases by approximately 33% and that oxidative metabolism increases by approximately 45% during neonatal seizures. Five babies had PCr/Pi ratios of less than 0.8 during seizures and subsequently developed long-term neurological sequelae, which suggests that neonatal seizures may cause or exacerbate cerebral injury by increasing cerebral metabolic demands above energy supply.
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PMID:Cerebral metabolic effects of neonatal seizures measured with in vivo 31P NMR spectroscopy. 378 67

Despite the widespread use of glucocorticoids in patients with severe head injury, the usefulness is still controversial. In the past, the effect was investigated only in terms of dose-response relationship. We have, however, studied the time factor for the administration of dexamethasone to obtain maximal beneficial effect together with investigating the influence of actinomycin-D, an inhibitor of messenger RNA synthesis, before dexamethasone treatment. Awake male mice of dd-strain were restrained and subjected to head injury using a bakelite weight of 30 g dropped from a height of 17.8 cm above the skull. This injury resulted in immediate loss of consciousness in 100%, convulsive seizure in about 70% and death in about 30% of animals. The severity of consciousness disturbance was evaluated by a pair of indices in time interval: time required for the recovery of righting reflex (RR) and for the recovery of spontaneous movement (SM). 4 mg/kg of dexamethasone phosphate was given intraperitoneally 0.5, 4, 6, 12, 18 or 24 hours before injury. Actinomycin-D of 0.5 mg/kg was injected intravenously 1 h before each dexamethasone treatment in separate animals. In the other group of animals, dose was changed with varying time course of dexamethasone pretreatment, e.g., 2, 4, 6 or 8 mg/kg given 0.5, 2 or 4 h before injury. It was found that dexamethasone of 4 mg/kg pretreatment 4-12 hours significantly improved the recovery from consciousness disturbance and death rate. Actinomycin-D given before dexamethasone treatment completely abolished the protective effect of dexamethasone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Time course of the cerebroprotective effect of dexamethasone in experimental head injury]. 382 51

A single intraperitoneal injection of pyridoxal-5'-phosphate (PLP) in a species of mouse, DBA/2J, that is normally susceptible to sound-induced convulsion exacerbated its epileptic condition. The effect of injection was most pronounced about 30 min after the administration and subsided gradually within the following 4 h. Correlated with this increased seizure susceptibility were enhanced levels of synaptosomal aspartate and glutamate, and a diminished gamma-aminobutyric acid (GABA) level. The concentrations of nonneuroactive amino acids remained unchanged. When stimulated with veratrine, synaptosomes prepared from PLP-injected mice showed an increased release of aspartate and glutamate and a decreased release of GABA compared to those prepared from control mice. The activity of glutamate decarboxylase in the brains of PLP-treated mice was lowered, whereas the activity of GABA-transaminase was enhanced. Finally, the epileptic condition of DBA mice could be ameliorated by maintenance on a diet composed of vitamin B6-deficient feed and cellulose.
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PMID:Alteration of amino acid metabolism in epileptogenic mice by elevation of brain pyridoxal phosphate. 398 38

The concentrations of pyridoxal 5'-phosphate in the brains of DBA/2J mice during the withdrawal period following chronic ethanol ingestion were measured fluorimetrically. The brain of the ethanol-withdrawn mouse contains 22.4 +/- 3.1% more pyridoxal 5'-phosphate than the brain of a control mouse. The enhanced susceptibility to epileptic seizures during the withdrawal phase may in part be due to the increased cerebral content of this coenzyme.
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PMID:Enhancement of brain pyridoxal 5'-phosphate level following chronic ingestion of ethanol. 408 33

The cerebral concentrations of pyridoxal-5'-phosphate and divalent transition metal ions (Cu2+ and Zn2+) are appreciably higher in the seizure-susceptible strain of mouse (DBA/2J) than those in normal strains (CBA/Ca and Parkes ). By injecting metal ions intracranially and pyridoxal-5'-phosphate intraperitoneally, we could render the normal mouse prone to sound-induced epilepsy. The behaviour of the treated seizure-susceptible strain of mouse. The levels of glutamate and aspartate in its inferior colliculus were elevated and the concentration of gamma-aminobutyrate was lowered. Glutaminase inhibitors, 6-diazo-5-oxo-L-norleucine (DON) and 0-diazo-acetyl-L-serine (azaserine), and a transaminase inhibitor, 4-amino-3- isoxazolidone (L-cycloserine), when injected intraperitoneally, protected the seizure-susceptible mouse from undergoing convulsions, whereas pyridoxal-5'-phosphate and methionine sulphoximine, a glutamine synthetase inhibitor, exacerbated its epileptic condition. We propose a possible sequence of biochemical events associated with susceptibility to audiogenic seizures.
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PMID:Studies on sound-induced epilepsy in mice. 614 59

Electrographic and clinical observations were made after the injection of kainic acid into the unilateral hippocampus of freely moving cats. Vehicle solution (phosphate buffer solution) for control study and kainic acid(1, 4 and 12 micrograms) were administered via a chronically implanted cannula. The control group showed no modification during the observation period. After the injection of 1 microgram of kainic acid, focal status epilepticus was observed for 2-3 days and then cats became normal afterwards. In the group of 4 micrograms kainic acid infection, cats demonstrated limbic status for 3 days, and persistent inter-ictal discharges continued during the observation period. Independent amygdaloid seizures and secondary generalized convulsions developed in the cats administered 12 micrograms of kainic acid. The cats died in the status epilepticus. The dose-dependent and substantial effect of KA without the influences of anesthesia and surgery was demonstrated. The results were discussed in relation to the human medial temporal sclerosis and the effects on the emotional mechanism of the limbic system. We suggest this model to be useful in the study of various types of temporal lobe epilepsy and the emotional mechanisms of the limbic system.
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PMID:Electroclinical features of kainic acid-induced status epilepticus in freely moving cats. Microinjection into the dorsal hippocampus. 617 56

Administration of pilocarpine or physostigmine to rats treated with lithium chloride produced sustained limbic seizures, widespread brain damage, and increased concentrations of D-myo-inositol-1-phosphate (a metabolite of the phosphoinositides, lipids involved in membrane receptor function) in the brain. The syndrome was preventable with atropine. The physostigmine doses and concentrations of blood lithium that caused the syndrome are similar to those considered appropriate for psychiatric chemotherapy.
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PMID:Systemic cholinergic agents induce seizures and brain damage in lithium-treated rats. 630 Oct 5


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