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

Ten ACT UP members will each receive $20,000 as a settlement of their claims against U.S. marshals. The AIDS activists were strip-searched following a demonstration at the Food and Drug Administration (FDA) office in Portland, OR. The search violated their Fourth Amendment rights to be free from unreasonable search and seizure. The activists were shackled and strip-searched in a semi-public area. The suit charged that the marshals' actions were degrading and intrusive. ACT UP will review how government training manuals respond to AIDS-related issues and situations.
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PMID:Ten activists get $20,000 each as a result of illegal strip search. 1136 81

Tamoxifen (TXF; an antiestrogen), cyproterone acetate (CYP; an antiandrogen) and mifepristone (MIF; an antigestagen) did not affect kindling parameters (afterdischarge threshold, seizure severity, seizure duration and afterdischarge duration) in fully-kindled rats. TXF (50 mg/kg) and CYP (50 mg/kg), when combined with carbamazepine, or phenobarbital, both antiepileptics administered at their highest subprotective doses of 15 mg/kg, resulted in significant reduction of the seizure and afterdischarge durations, both in male and female rats. Additionally, the combination of carbamazepine and cyproterone markedly increased the afterdischarge threshold in fully-kindled rats of both genders. The interaction between antihormones and carbamazepine, or phenobarbital, was not reversed by the respective gonadal hormones (estradiol, progesterone, and testosterone), kainic acid, or strychnine. However, the TXF-, and CYP-induced effect on the action of carbamazepine was abolished by bicuculline, N-methyl-D-aspartic acid and aminophylline. The effect of TXF on the protective activity of phenobarbital was reversed by bicuculline and N-methyl-D-aspartic acid. Finally, the CYP-mediated effect on phenobarbital action was abolished by bicuculline and aminophylline. Neither TXF nor CYP altered free plasma levels and brain levels of carbamazepine or phenobarbital, so a pharmacokinetic interaction between antihormones and antiepileptic drugs is not probable. In view of the present data, it may be suggested that the protective activity of the antiestrogen and antiandrogen are mostly associated with the enhancement of GABA-ergic and purinergic transmission in the central nervous system. Also the augmentation of glutamatergic transmission, realized through NMDA receptors, may be involved in the mechanism of antiseizure action of TXF and CYP.
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PMID:Effect of antihormones in amygdala-kindled seizures in rats. 1178 14

A 24-year-old woman with overlapping features of sclerodermia sine scleroderma and systemic lupus erythematosus (SLE) presented with rapidly accelerating hypertension accompanied by neuropsychological deficits and tonic-clonic seizures. Kidney biopsy showed severe intimal hyperplasia of small renal arteries but no glomerulonephritis. Following treatment with ACE inhibitor, prednisolone and cyclophosphamide complete remission was achieved with minimal brain damage and normal kidney function. Anti-RNA polymerase I, II and III antibodies have remained positive during follow-up for 2 years, suggesting a linkage with the underlying pathogenetic pathway.
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PMID:Renal crisis in asclerodermic scleroderma--lupus overlap syndrome. 1178 81

In the brain, acetate is exclusively oxidized by glia. To determine the contribution of glial metabolism to the tricarboxylic acid cycle (TCA), 1-(13)C-acetate was infused in six studies in three normal adult subjects and -one epileptic receiving valproic acid for seizure control. Ten grams of 99% 1-(13)C labeled acetate were infused intravenously as a 3.3% w/v solution over 60 min, during which in vivo 13C MR spectra of the brain were acquired. As expected, 13C label rapidly enriched cerebral bicarbonate, glutamate and glutamine C5. The mean rate of acetate oxidation calculated from steady-state 13C enrichment of bicarbonate in fasted normal subjects was 0.13 +/- 0.03 micromol/g/min (n=4), approximately 20% of the total cerebral TCA cycle rate.
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PMID:Tricarboxylic acid cycle of glia in the in vivo human brain. 1184 May 47

Fas, (APO-1/CD95), a transmembrane glycoprotein belonging to the tumor necrosis (TNF) receptor superfamily, transduces apoptotic death upon crosslinking by its cognate ligand (FasL). As upregulation of Fas/FasL expression occurs in neuropathological conditions (e.g., stroke, central nervous system [CNS] trauma and seizures) associated with oxidative damage, we questioned whether reactive oxygen species (ROS) can directly affect Fas and FasL expression in neuronal cells. Utilizing rat PC12 cells neuronally differentiated with nerve growth factor (NGF), we observed that concentrations of H(2)O(2) inducing apoptotic cell death rapidly trigger the expression of Fas mRNA and protein as well as FasL mRNA. Although NGF-addition to naive PC12 downregulated constitutive Fas and FasL transcription, the H(2)O(2)-induced Fas and FasL mRNA upregulation invariably occurred either in the presence or in the absence of NGF. Similarly, phorbol 1,2-myristate 1, 3-acetate (PMA), a potent protein kinase C (PKC) activator, did not modify Fas and FasL mRNA upregulation subsequent to H(2)O(2) exposure. On the contrary, forskolin and dibutyryl cAMP, which elevate intracellular cAMP by independent mechanisms, both counteracted H(2)O(2)-induced Fas, but not FasL, mRNA upregulation and increased constitutive expression of FasL mRNA. Altogether, our data show that oxidative stress is a major stimulus in eliciting Fas and FasL expression in NGF-differentiated PC12 cells. Moreover, we describe here for the first time the existence of cAMP-dependent mechanism(s) modulating Fas and FasL expression.
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PMID:H(2)O(2) induces upregulation of Fas and Fas ligand expression in NGF-differentiated PC12 cells: modulation by cAMP. 1211 99

Seizure activity associated with cortical dysplasia (CD) is often resistant to standard pharmacologic treatments. Although several animal models exhibit CD, virtually nothing is known about antiepileptic drug (AED) responses in these animals. Here we have used rats exposed to methylazoxymethanol acetate (MAM) in utero, an animal model featuring nodular heterotopia, to investigate the effects of AEDs in the dysplastic brain. 4-aminopyridine (100 microM), a K(+) channel blocker, was used to induce interictal epileptiform bursting in acute hippocampal slices from MAM-exposed and age-matched vehicle-injected control animals. Extracellular field recordings were used to monitor seizure activity in vitro. Five commonly used AEDs were tested: phenobarbital, 25-400 microM; carbamazepine, 25-200 microM; valproate (VPA), 0.19-4 mM; ethosuximide (ESM), 0.5-8 mM; and lamotrigine (LTG), 49-390 microM. 4-AP-induced bursting occurred with shorter latencies in slices from MAM-exposed rats in comparison with slices from controls, confirming the intrinsic hyperexcitability of dysplastic tissue. Each AED tested demonstrated significant burst suppression in control slices, but interictal epileptiform bursting in MAM-exposed slices was resistant to these treatments. Even at the highest concentrations, VPA, ESM and LTG had no effect on burst amplitude in slices from MAM-exposed rats. Pharmaco-resistance was further tested by measuring seizure latencies in awake, freely-moving rats after kainate administration (15 mg/kg, i.p.) with and without pre-treatment with VPA (400 mg/kg i.p.). Pre-treatment with VPA prolonged seizure latency in control rats, but had no effect in MAM-exposed animals. These results suggest MAM-exposed rats exhibit a dramatically reduced sensitivity to commonly prescribed AEDs.
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PMID:Effects of antiepileptic drugs on induced epileptiform activity in a rat model of dysplasia. 1220 Feb 16

Limbic seizures were induced in rats by intraperitoneal injection of the glutamate receptor agonist kainic acid, followed, 24h later by injection of [1-13C]glucose and [1,2-13C]acetate. Analyses of forebrain extracts were performed using 13C magnetic resonance spectroscopy and HPLC. A significant increase in label derived from [1,2-13C]acetate was observed in glutamine and glutamate. Label in most metabolites derived from [1-13C]glucose was unchanged, however, a decrease was observed in [2-13C]GABA, possibly due to reduced GABA release, 24h after kainic acid injection. It should be noted that only astrocytes are able to utilize acetate as a substrate efficiently, whereas acetyl CoA derived from glucose is metabolized predominantly in the neuronal tricarboxylic acid cycle. No significant differences were found in total amounts of amino acids between the two groups. Thus, these results indicate that turnover of metabolites was increased predominantly in astrocytes whereas glutamatergic neurons were not affected. Previous results obtained using the same model [Neurosci. Lett. 279 (2000) 169] showed an increased turnover in both glutamatergic and GABAergic neurons 2 weeks after kainic acid injection. Combining the results from the two studies, it can be suggested that increased astrocytic activity 1 day after epileptic seizures results, subsequently, in an increased amino acid turnover in neurons.
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PMID:Glial-neuronal interactions following kainate injection in rats. 1244 Nov 74

3 alpha-Hydroxy-6,19-oxidopregn-4-ene-20-one (4) was prepared in seven steps from pregnanolone acetate. At 0.1 microM concentration 4 significantly increased GABA induced (36)Cl(-) influx in hamster cerebral cortex synaptoneurosomes while at 20 mg/kg it decreased the percentage of hamsters showing seizures induced by 3-mercaptopropionic acid.
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PMID:Synthesis and GABA(A) receptor activity of a 6,19-oxido analogue of pregnanolone. 1256 26

Seizures were induced in rats by intraperitoneal injection of pentylenetetrazole (PTZ, 70 mg/kg), followed, 30 min later, by injection of [1-13C]glucose and [1,2-13C]acetate. Analyses of extracts from cortex, subcortex and cerebellum were performed using 13C magnetic resonance spectroscopy and HPLC. It could be shown that PTZ affected different brain regions differently. The total amounts of glutamate, glutamine, GABA, aspartate and taurine were decreased in the cerebellum and unchanged in the other brain regions. GABAergic neurones in the cortex and subcortex were not affected, whereas those in the cerebellum showed a pronounced decrease of GABA synthesis. However, glutamatergic neurones in all brain regions showed a decrease in glutamate labelling and in addition a decreased turnover in cerebellum. It could be shown that this decrease was in the metabolic pool of glutamate whereas release of glutamate was unaffected since glutamine labelling from glutamate was unchanged. Aspartate turnover was also decreased in all brain regions. Changes in astrocyte metabolism were not detected, indicating that PTZ had no effect on astrocyte metabolism in the early postictal stage.
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PMID:Pentylenetetrazole decreases metabolic glutamate turnover in rat brain. 1275 79

Genetic and epigenetic factors may alter the normal development of cerebral cortex, producing laminar and cellular abnormalities and heterotopiae, major causes of juvenile, drug-resistant epilepsy. Experimentally-induced migration disorders provide interesting insights in the mechanisms of the determination of neuronal phenotype and connectivity, of congenital cortical dysgenesis and the pathophysiology of associated neurological disorders, such as epilepsy. We investigated the effects of E14 administration of methylazoxymethanol acetate (MAM), which induces microencephaly by ablating dividing cells. Brains from newborn and adult rats were reacted for NADPH-d and CO histochemistry. Moreover, callosally-projecting neurons were retrogradely labeled with DiI at P9 or with BDA in adults. MAM-treated rats displayed a remarkable reduction in cortical thickness, mainly due to reduction in layer IV and in supragranular layers. Heterotopic nodules appeared in the supragranular layers and in the hippocampus. CO-positive barrels in somatosensory cortex were almost absent. The distribution of NADPH-d-positive neurons was regular, but they were rare in heterotopic nodules. Callosally-projecting neurons displayed abnormal orientation of the apical dendrite and increase in the basal dendritic length. Alterations in the dendritic arborization of pyramidal neurons may be one of the substrates for the increased sensitivity to drugs which induce epileptic seizures in these animals.
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PMID:Experimentally-induced microencephaly: effects on cortical neurons. 1278 21


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