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phosphatidic acid/crise épileptique
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[Metabolism of neuronal and neuroglial phospholipids in seizures].
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Metabolism of individual phospholipids was studied in neurones and neuroglia under conditions of convulsions caused by picrotoxin administration. Metabolic activity of all the phospholipids studied was increased in neuronal membranes under extreme conditions of convulsive attacks. The rate of
Picrotoxin-induced convulsions alters rat brain microsomal membrane structural properties.
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Cerebral microsomal membrane properties were assessed in the chronic condition of generalized seizure induced by picrotoxin (PTX) in rats. PTX-induced seizures resulted in increased lysophosphatidyl glycerol, phosphatidylcholine and phosphatidic acid components, while phosphatidylethanolamine,
Effect of various drugs producing convulsive seizures on rat brain glycerolipid metabolism.
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Convulsive seizures were elicited in the rat by the injection of several different drugs (pyridoxal phosphate, bicuculline, penicillin and ouabain). Glycerolipid metabolism was studied after the intraventricular injection of [2-3H]glycerol, which was incorporated into rat brain glycerides. The
Cerebral phosphoinositide, triacylglycerol and energy metabolism during sustained seizures induced by bicuculline.
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In ventilated rats, levels of phosphatidylinositol (PI), phosphatidylinositol 4-phosphate (PIP), phosphatidylinositol 4,5-bisphosphate (PIP2), diacylglycerol (DAG), triacylglycerol (TAG), free fatty acids (FFA) and phosphatidic acid, as well as their fatty acid contents, were measured in forebrain
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
Metabolic, Reproductive, and Neurologic Abnormalities in Agpat1-Null Mice.
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Defects in the biosynthesis of phospholipids and neutral lipids are associated with cell membrane dysfunction, disrupted energy metabolism, and diseases including lipodystrophy. In these pathways, the 1-acylglycerol-3-phosphate O-acyltransferase (AGPAT) enzymes transfer a fatty acid to the sn-2
Recent progress on type II diacylglycerol kinases: the physiological functions of diacylglycerol kinase δ, η and κ and their involvement in disease.
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Diacylglycerol kinase (DGK) phosphorylates diacylglycerol (DAG) to produce phosphatidic acid (PA) and plays an important role in signal transduction by modulating the balance between these signalling lipids. To date, 10 mammalian DGK isozymes have been identified, and these isozymes are subdivided
Diacylglycerol kinases as emerging potential drug targets for a variety of diseases.
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Diacylglycerol (DAG) kinase (DGK) modulates the balance between the two signaling lipids, DAG and phosphatidic acid (PA), by phosphorylating (consuming) DAG to yield PA. Ten mammalian DGK isozymes have been identified to date. In addition to two or three cysteine-rich C1 domains (protein kinase
Activity-dependent translocation of neurogranin to neuronal nuclei.
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Long-term changes of synaptic plasticity depend on protein synthesis and transcription. Ng (neurogranin) is a small protein concentrated at dendrites and spines of forebrain neurons, involved in synaptic plasticity through the regulation of CaM (calmodulin)-mediated signalling. Ng presents a central
Enhanced inositide turnover in brain during bicuculline-induced status epilepticus.
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Because brain inositides are enriched in the 1-stearoyl-2-arachidonoyl species, they form a likely source for the tetraenoic free fatty acids (FFA) and diacylglycerols (DG) that are accumulated during seizures. To study inositide turnover during bicuculline-induced seizures, rats were injected
Diacylglycerol kinase epsilon modulates rapid kindling epileptogenesis.
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OBJECTIVE
Diacylglycerol kinase epsilon (DGKepsilon) regulates seizure susceptibility and long-term potentiation through arachidonoyl-inositol lipid signaling. We studied the significance of arachidonoyl-diacylglycerol (20:4 DAG) in epileptogenesis in DGKepsilon-deficient mice undergoing rapid
Expression, Purification, and Characterization of Human Diacylglycerol Kinase ζ.
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Diacylglycerol kinase ζ (DGKζ) phosphorylates diacylglycerol (DG) to generate phosphatidic acid. The dysfunction of DGKζ has been linked to several diseases, such as cardiac hypertrophy, ischemia, and seizures. Moreover, much attention has been paid to DGKζ, together with DGKα, as a potential target
Mechanism of depression of brain phospholipid levels by an epileptogenic drug.
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Treatment of the rat with U18666A [3 beta-(2-diethylaminoethoxy) androst-5-en-17-one HCl] resulted in development of a chronic seizure state and 20-40% reductions in the concentration of all major phospholipid in whole brain. The mechanism of the phospholipid changes was explored in the present
Epileptogenesis in diacylglycerol kinase epsilon deficiency up-regulates COX-2 and tyrosine hydroxylase in hippocampus.
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Diacylglycerol kinase (DGK) phosphorylates the second messenger diacylglycerol (DAG) to yield phosphatidic acid, two neural signaling elements that function to modulate synaptic activity. Of the nine mammalian DGK isotypes known, DGK epsilon (DGKepsilon) shows specificity for
A Case of 22q11 Deletion Syndrome (22q11DS) with a Panayiotopoulos Epileptic Pattern: Are Additional Copy-Number Variations a Possible Second Hit in Modulating the 22q11DS Phenotype?
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"22q11 deletion syndrome" (22q11DS) is a rare genetic syndrome, in which most patients share the same deletion, but their clinical features may vary a great deal. The genetic mechanisms underlying the variable expressivity and reduced penetrance of 22q11DS still have to be fully elucidated. Epilepsy
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