Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of calcium hydroxide on the maximal seizure threshold was studied in 18-day-old rats using the up-and-down method. The maximal seizure was induced by administering an electric shock through the eyes. When calcium hydroxide was given orally once a day (0.04 m moles/kg) for 10 days from the 8th to 18th day after birth, the maximal seizure threshold was raised by 4.8 mA, which corresponded to 16% of the threshold current in the control. the serum calcium concentration was not significantly altered after the treatment. When calcium chloride was given intraperitoneally, the maximal seizure threshold markedly increased with the increase in serum calcium. It is suggested that the mechanism of calcium hydroxide is different from that induced by increasing the serum calcium.
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PMID:Elevation of the maximal seizure threshold produced by calcium hydroxide in rats. 731 Nov 41

Several 1,1-bis(4-alkyl/aryl-1,2,4-triazoline-5-thione-3-yl)-2- methylbutane derivatives 13-21 were obtained from the cyclization of mono(1-methylpropyl)malonylbis(4-alkyl/aryl)thiosemicarbazides 2-12 in the presence of sodium hydroxide. Their chemical structures were proven by spectral data (UV, IR, 1H-NMR, MS) and elemental analysis. The anticonvulsant activity of the title compounds were determined against pentylenetetrazole induced seizures. Six of the tested compounds showed anticonvulsant activity (10 to 20% protection).
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PMID:Synthesis and anticonvulsant activity of some new 1,1-bis(4-substituted 1,2,4-triazoline-5-thione-3-yl)-2-methylbutanes. 775 67

The role of GABAb receptor activation in the expression of both interictal and ictal phenomena was investigated in slices of area CA3 of the rat hippocampal formation. Interictal-like bursts occurred following application of high frequency trains to the Schaffer collaterals. When two bursts were triggered using paired stimuli, profound depression of the second burst was seen 150-600 ms following the first burst. GABAb receptor antagonists potently reversed the paired pulse depression of the interictal-like bursts. Reversal of the paired depression was also accomplished by increasing the extracellular concentration of K+ by 2-3 mM. Additional experiments were performed in area CA3 to determine the role of GABAb receptor activation on the expression of ictal phenomena. Electrographic seizures (EGSs) were induced by application of high frequency trains. 2-Hydroxy-saclofen (200 microM) significantly decreased the duration of trains required to elicit EGSs. Taken together, these data suggest that GABAb receptor activation has potent inhibitory effects on both ictal and interictal-like events.
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PMID:Antiepileptic effects of GABAb receptor activation in area CA3 of rat hippocampus. 838 98

The effects of trimethyltin on the hippocampus were investigated in terms of changes in histology, depth electroencephalography, learning acquisition and memory retention, choline acetyltransferase and neuropeptides, and seizure-induced c-fos messenger RNA expression. The results were as follows. (1) Morphologically, trimethyltin produced a progressive loss of hippocampal CA3 and CA4 pyramidal cells, starting from four days after peroral treatment with trimethyltin hydroxide (9 mg/kg), as described previously. (2) Neurophysiologically, the increased seizure susceptibility to pentylenetetrazol treatment reached a maximum at four days post-trimethyltin and then declined after five days post-trimethyltin. The maximal seizure susceptibility at four days post-trimethyltin was confirmed by the immediate and long-lasting appearance of spike discharge in the hippocampus. However, this was not verified by the expression of c-fos messenger RNA in the hippocampus, which was comparable between trimethyltin-treated and control rats. (3) Behaviorally, the time-courses of aggression and learning impairment were similar to that of the seizure susceptibility. (4) Neurochemically, trimethyltin treatment caused changes of neurochemical markers, which were manifested by the elevation of neuropeptide Y content in the entorhinal cortex, and of choline acetyltransferase in the hippocampal CA3 subfield. Trimethyltin may offer potential as a tool for investigations on the relationship between neuronal death in the hippocampus and the development of seizure susceptibility and learning impairment. Alterations in glucocorticoids, glutamate and neuropeptides may all contribute to the manifestation of the trimethyltin syndrome.
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PMID:Trimethyltin syndrome as a hippocampal degeneration model: temporal changes and neurochemical features of seizure susceptibility and learning impairment. 933 Mar 76

In situ hybridization and immunocytochemistry were applied to investigate changes in the expression of somatostatin, neuropeptide Y, neurokinin B, cholecystokinin, dynorphin, and Met-enkephalin in the rat hippocampus after administration of a single peroral dose of trimethyltin hydroxide (9 mg/kg). Two time intervals were investigated: 5 days after trimethyltin treatment, when CA3 damage becomes manifest and is associated with increased aggression, seizure susceptibility, and memory deficit, and 16 days after trimethyltin, when neuronal damage is almost maximal and seizure susceptibility is declining. Robust but transient increases of neuropeptide Y, neurokinin B, and Met-enkephalin mRNA levels were revealed in the granule cell layer of the dentate gyrus and increased neuropeptide Y and neurokinin B immunoreactivities were found in mossy fibers. In reverse, dynorphin mRNA and immunoreactivity were decreased transiently in the dentate gyrus and mossy fibers, respectively. Strong over-expression of NPY mRNA was also observed in hilar interneurons and in CA1 and CA3 pyramidal cells as well as in the cortex at 5 days postdosing. Cholecystokinin- or neurokinin B-containing basket cells were preserved, while somatostatin-bearing interneurons were damaged by trimethyltin exposure. These neurochemical changes induced by trimethyltin intoxication strikingly parallel to those observed in animal models of temporal lobe epilepsy and may reflect activation of endogenous protective mechanisms. It is also suggested that hilar interneurons respond differently to trimethyltin exposure, for which neuropeptides are valuable markers.
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PMID:Trimethyltin intoxication induces marked changes in neuropeptide expression in the rat hippocampus. 966 Dec 51

A six-month-old, intact female Himalayan kitten was presented to the University of Tennessee Veterinary Medical Teaching Hospital for evaluation of chronic lethargy, inappetance, muscle tremors, and seizures. Upon physical examination, the kitten was very small for her age. Bilateral, incipient-to-immature cataracts were seen on ophthalmic examination. Severe hypocalcemia and concurrent hyperphosphatemia were identified on initial diagnostic evaluation. A diagnosis of primary hypoparathyroidism was made by identifying reduced concentrations of parathyroid hormone (PTH). The kitten responded well to treatment with calcium, vitamin D, and aluminum hydroxide and is clinically normal 17 months after initiation of treatment.
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PMID:Hypocalcemia and hyperphosphatemia due to primary hypoparathyroidism in a six-month-old kitten. 982 87

3-Hydroxy-3-Methylglutaryl coenzyme A lyase (HMG-CoA) deficiency is a rare inborn error of leucine catabolism. The disease is characterized by recurrent episodes of metabolic acidosis, hyperammonemia without ketosis, hypoglycemia, lethargy, hepatomegaly, and seizures. This study has evaluated the magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) findings of three patients with HMG-CoA deficiency. The common findings on all of the MRI scans were multiple, coalescent, marked lesions in periventricular white matter and arcuate fibers, most prominently in frontal or periatrial regions that were superimposed on diffuse, slightly hyperintense subcortical white matter signal. Involvement of the caudate nucleus and the dentate nucleus were observed in the reported patients. MRS studies by both STEAM and PRESS spectra of all patients revealed a decrease in N-acetylaspartate and elevation in both myoinositol and choline. A pathologic peak at 1.33 ppm, which is compatible with lactate, and a particular peak at 2.42 ppm in all patients were also found. The combination of both MRI and MRS findings could be considered as being specific in patients with HMG-CoA lyase deficiency.
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PMID:MRI and MRS in HMG-CoA lyase deficiency. 1037 84

We examined the effect of dipotassium clorazepate (7-chloro-1, 3-dihydro-2-oxo-5-phenyl-1H-1, 4-benzodiazepine-3-carboxylate potassium hydroxide), an antianxiety drug, on amygdaloid kindling and compared its effects for 7 successive days on amygdaloid- versus hippocampal-kindled seizures, using the rat kindling model of epilepsy. Dipotassium clorazepate at 5 mg/kg significantly delayed amygdaloid kindling. The contralateral cortical after-discharge duration in the dipotassium clorazepate-treated group was significantly shorter than the after-discharge duration in the amygdala in the first seven stimulations, whereas it was significantly shorter only in the first three stimulations in the control group, indicating that dipotassium clorazepate suppressed the spread of seizure activity from focus to contralateral cortex. Dipotassium clorazepate suppressed amygdaloid-kindled seizures at 2 and 5 mg/kg, while 1 mg/kg or more suppressed hippocampal-kindled seizures. Thus, differences in effective dosages in both amygdaloid- and hippocampal-kindled seizures may suggest a difference in the neuronal mechanisms involved in this kindling.
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PMID:Effect of dipotassium clorazepate on amygdaloid-kindling and comparison between amygdaloid- and hippocampal-kindled seizures in rats. 1060 66

The objective of this study was to determine the role of mitochondrial superoxide radical-mediated oxidative damage in seizure-induced neuronal death. Using aconitase inactivation as an index of superoxide production, we found that systemic administration of kainate in rats increased mitochondrial superoxide production in the hippocampus at times preceding neuronal death. 8-Hydroxy-2-deoxyguanosine, an oxidative lesion of DNA, was also increased in the rat hippocampus following kainate administration. Manganese(III) tetrakis(4-benzoic acid)porphyrin, a catalytic antioxidant, inhibited kainate-induced mitochondrial superoxide production, 8-hydroxy-2-deoxyguanosine formation and neuronal loss in the rat hippocampus. Kainate-induced increases of mitochondrial superoxide production and hippocampal neuronal loss were attenuated in transgenic mice overexpressing mitochondrial superoxide dismutase-2. We propose that these results demonstrate a role for mitochondrial superoxide production in hippocampal pathology produced by kainate seizures.
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PMID:Mitochondrial superoxide production in kainate-induced hippocampal damage. 1111 5

The reproducibility of a method developed to evaluate point-of-use sanitizers for fresh produce was tested at three different laboratories. Mixtures of five Salmonella serotypes were inoculated on the surface of ripe tomatoes. After the inoculum was dry, tomatoes were placed inside a plastic bag and sprayed with sterile USP water, Dey and Engley (D/E) neutralizer broth, or a prototype Fit produce wash (PW), an alkaline solution comprised of generally recognized as safe ingredients (water, oleic acid, glycerol, ethanol, potassium hydroxide, sodium bicarbonate, citric acid, and distilled grapefruit oil), and rubbed for 30 s. The tomatoes were rinsed 10 s with 195 ml of D/E neutralizer broth (rinse solution), then combined with 20 ml of D/E neutralizer (residual wash solution) and rubbed by hand to remove residual Salmonella. Populations of Salmonella were determined for each tomato in the rinse solution and residual wash solution. Treatment with PW resulted in reductions in the number of Salmonella 2 to 4 logs greater than those achieved with the sterile water or D/E neutralizer broth controls. Consistent results were obtained across the three study sites, indicating reproducible results were obtained using the test method. The method used to determine the efficacy of killing or removing Salmonella from tomatoes in this study is suggested as a standard method for measuring the efficacy of sanitizers on tomatoes and other similar fruits and vegetables with rigid, smooth surfaces.
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PMID:Efficacy and reproducibility of a produce wash in killing Salmonella on the surface of tomatoes assessed with a proposed standard method for produce sanitizers. 1160 93


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