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Pagina 1 a partire dal 175 risultati
Inositol trisphosphate (IP3) receptors and epileptic seizure.
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The effects of anticonvulsants and Ca2+ channel antagonists on the inositol trisphosphate (IP3) binding and IP3-induced Ca2+ release were examined in brain membrane fractions. Anticonvulsant (PHT and valproate) and Ca2+ channel antagonists (verapamil, diltiazem, flunarizine, nicardipine and
Sustained effects of pilocarpine-induced convulsions on brain inositol and inositol monophosphate levels and brain morphology in young and old male rats.
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Cerebral inositol and inositol monophosphates, products of phosphoinositide (PI) turnover, and neuronal injury were studied in young (10 weeks) and old (24 months) male Wistar rats after pilocarpine-induced convulsions. The goal was to explore the association between short-term cholinergic
Restoration of brain myo-inositol levels in rats increases latency to lithium-pilocarpine seizures.
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Lithium pretreatment in rats potentiates the epileptogenic effects of pilocarpine and other cholinergic agonists. In order to determine if this effect of lithium could be reversed by myo-inositol, rats were pretreated with intracerebroventricular (ICV) injections of myoinositol, artificial CSF or
Crystal structure of human myo-inositol monophosphatase 2, the product of the putative susceptibility gene for bipolar disorder, schizophrenia, and febrile seizures.
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The human IMPA2 gene, which encodes myo-inositol monophosphatase 2 (IMPA2), is mapped onto 18p11.2, a susceptibility region for bipolar disorder. This chromosomal region has also been proposed to include a susceptibility locus for schizophrenia and febrile seizures. Here we report the crystal
Kainic acid-induced seizure upregulates Na(+)/myo-inositol cotransporter mRNA in rat brain.
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A major organic osmolyte, myo-inositol protects cells from perturbing effects of high intracellular concentrations of electrolytes. Myo-inositol is accumulated into cells through Na(+)/myo-inositol cotransporter (SMIT). In order to investigate the regulation of SMIT in generalized seizure, we
Soman-induced convulsions affect the inositol lipid signaling system: potentiation by lithium; attenuation by atropine and diazepam.
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Effects of atropine or diazepam pretreatment on soman-induced convulsions and brain phosphoinositide (PI) metabolism, as assessed by brain regional inositol-1-phosphate (IP1) levels, were studied in saline and LiCl-pretreated rats. IP1, an intermediate in PI turnover, was measured in cortex,
Convulsions and cerebral inositol-1-phosphate levels in rats treated with diisopropyl fluorophosphate.
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In order to examine the relationship of organophosphate-induced cholinergic stimulation to phosphoinositide (PI) hydrolysis in the brain, diisopropyl fluorophosphate (DFP; 1.3 or 1.5 mg/kg subcutaneously) was given to rats pretreated with saline or LiCl (5 meq/kg subcutaneously). Behaviour was
Effect of kainic acid-induced status epilepticus on inositol-trisphosphate and seizure-induced brain damage in mature and immature animals.
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We investigated the role of excitatory amino acids in the activation of the phosphoinositide pathway during kainic acid-induced seizures in mature and immature animals. Kainic acid caused more severe seizures in the immature animals, but no hippocampal damage or induction of phosphoinositide
Modulation by inositol of cholinergic- and serotonergic-induced seizures in lithium-treated rats.
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Hippocampal and cortical EEG recordings in rats were used to monitor the in vivo modulation by lithium of responses to agonists for 5HT2/5HT1c serotonergic (DOI) and cholinergic (pilocarpine) receptors and the influence of inositol administration. Administration of DOI (8 mg/kg) or pilocarpine (30
Inositol trisphosphate, cyclic AMP, and cyclic GMP in rat brain regions after lithium and seizures.
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The mechanism of action of lithium, the primary treatment for bipolar affective disorder, is unknown but may involve inhibition of second messenger production in the brain. Therefore, the concentrations of three second messengers, inositol 1,4,5 trisphosphate (Ins 1,4,5P3), cyclic adenosine
Ataxia and epileptic seizures in mice lacking type 1 inositol 1,4,5-trisphosphate receptor.
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The inositol 1,4,5-trisphosphate (InsP3) receptor acts as an InsP3-gated Ca2+ release channel in a variety of cell types. Type 1 InsP3 receptor (IP3R1) is the major neuronal member of the IP3R family in the central nervous system, predominantly enriched in cerebellar Purkinje cells but also
Anticonvulsant activities of myo-inositol and scyllo-inositol on pentylenetetrazol induced seizures.
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Myo-inositol (MI) and its isomers are used for the treatment of various neuropathological conditions. The purpose of the present research was to study anticonvulsant properties of MI and scyllo-inositol (SCI) on pentylenetetrazol (PTZ) induced seizures in rats. Half an hour after treatment with MI
Effect of myo-inositol on convulsions induced by pentylenetetrazole and kainic acid in rats.
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We studied the effect of myo-inositol on pentylenetetrazole and kainic acid-induced seizures in rats. Myo-inositol significantly reduced seizure activity.
Cerebral and portal vein thrombosis, macrocephaly and atypical absence seizures in Glycosylphosphatidyl inositol deficiency due to a PIGM promoter mutation.
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Defects of the glycosylphosphatidylinositol (GPI) biosynthesis pathway constitute an emerging subgroup of congenital disorders of glycosylation with heterogeneous phenotypes. A mutation in the promoter of PIGM, resulting in a syndrome with portal vein thrombosis and persistent absence seizures, was
Diacylglycerol kinase epsilon regulates seizure susceptibility and long-term potentiation through arachidonoyl- inositol lipid signaling.
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Arachidonoyldiacylglycerol (20:4-DAG) is a second messenger derived from phosphatidylinositol 4,5-bisphosphate and generated by stimulation of glutamate metabotropic receptors linked to G proteins and activation of phospholipase C. 20:4-DAG signaling is terminated by its phosphorylation to
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