diacylglycerol/seizures

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Regional and temporal variations in the accumulation of unesterified fatty acids and diacylglycerols in the rat brain during kainic acid induced limbic seizures.

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These experiments tested the hypothesis that limbic seizures induced by kainic acid (KA) activate mechanisms (e.g. phospholipase) that degrade the cell membrane, causing a release and accumulation of free fatty acids (FFAs) and diacylglycerols (DGs) in brain areas susceptible to seizure-related

Circannual rhythm of free fatty acids and diacylglycerols in 5-day-old rat cerebrum during pentylenetetrazol-induced convulsions.

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Free fatty acids (FFA) and diacylglycerol (DG) content and composition in the cerebrum of 5-day-old rats were studied after pentylenetetrazol (PTZ)-induced convulsions. A threefold increase in brain FFA was observed 30 min after PTZ injection in experiments carried out in spring. In contrast, a 50%

Free fatty acid and diacylglycerol accumulation in the rat brain during recurrent seizures is related to cortical oxygenation.

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Cerebral blood flow and oxygenation increase during the early seizures of a series, but the increase in cerebral blood flow attenuates during late seizures, sometimes resulting in decreased cortical oxygenation. Cortical free fatty acids (FFA) and diacylglycerols also increase during early seizures

Disruption of diacylglycerol kinase delta (DGKD) associated with seizures in humans and mice.

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We report a female patient with a de novo balanced translocation, 46,X,t(X;2)(p11.2;q37)dn, who exhibits seizures, capillary abnormality, developmental delay, infantile hypotonia, and obesity. The 2q37 breakpoint observed in association with the seizure phenotype is of particular interest, because

Excitotoxicity by kainate-induced seizure causes diacylglycerol kinase ζ to shuttle from the nucleus to the cytoplasm in hippocampal neurons.

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Diacylglycerol kinase (DGK), which consists of several isozymes, plays a pivotal role in lipid second-messenger diacylglycerol metabolism. A nuclear isozyme, DGKζ, which is translocated from the nucleus to the cytoplasm in hippocampal neurons under transient ischemic stress, is implicated in nuclear

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

Membrane lipid degradation is related to interictal cortical activity in a series of seizures.

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Brain levels of free fatty acids (FFA) and diacylglycerols (DAG) rise rapidly with the onset of seizures, reflecting activation of phospholipases A2 (PLA2) and C (PLC), respectively. However, the ictal/interictal accumulation of FFA attenuates as recurrent seizures continue. To assess the role of

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

Second messengers in cholinergic-induced convulsions and neuronal injury.

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Acetylcholine (ACh) is a powerful excitatory neurotransmitter in the brain. Stimulation of brain cholinergic muscarinic receptors (mAChR) cause persistent tonic-clonic convulsions. mAChRs are coupled to G-protein which mediates the receptor stimulation to phospholipidase C (PLC). PLC hydrolyses

Asymmetry of diacylglycerol metabolism in rat cerebral hemispheres.

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Diacylglycerols (DGs) were found to be asymmetrically distributed between the two cerebral hemispheres of rat brain. The left cerebral hemisphere (LCH) contained 100% more DG than the right cerebral hemisphere (RCH). The lateralization was enhanced in animals subjected to depolarization induced by a

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

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

The accumulation of free arachidonic acid, diacylglycerols, prostaglandins, and lipoxygenase reaction products in the brain during experimental epilepsy.

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There has been increasing biochemical evidence since 1970 that one of the targets for convulsion-induced changes is the cell membrane of neurons. This is partly based on the observation that following seizures, there are increased levels of diacylglycerols and free fatty acids, which are products of

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

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