phospholipase/seizures

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Differential expression of phospholipase D isozymes in the hippocampus following kainic acid-induced seizures.

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To investigate the pathophysiological role of phospholipase D (PLD)-mediated signaling, changes in the expression of the PLD isozymes PLD1 and PLD2 were investigated in the rat kainic acid (KA) model of human temporal lobe epilepsy. Western blot analysis showed a significant increase in the

Secreted phospholipase A2-induced neurotoxicity and epileptic seizures after intracerebral administration: an unexplained heterogeneity as emphasized with paradoxin and crotoxin.

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After intracerebral injection, some toxic secreted phospholipases A2 (sPLA2) can induce epileptic seizures which bases are currently ill known. We undertook the detailed study of the central neurotoxicity of paradoxin (PDX), an analog of taipoxin, in rodents. Since literature strongly suggests a

Deletion of phospholipase C beta4 in thalamocortical relay nucleus leads to absence seizures.

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Absence seizures are characterized by cortical spike-wave discharges (SWDs) on electroencephalography, often accompanied by a shift in the firing pattern of thalamocortical (TC) neurons from tonic to burst firing driven by T-type Ca(2+) currents. We recently demonstrated that the phospholipase C

Phospholipase D1-promoted release of tissue plasminogen activator facilitates neurite outgrowth.

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Temporal lobe epilepsy (TLE) is the most common form of epilepsy, affecting approximately 1-2% of the population. Seizure events resulting from TLE are characterized by aberrant hippocampal mossy fiber sprouting and plastic responses that affect brain function. Seizure susceptibility is modulated by

Seizures increase acetylcholine and choline concentrations in rat brain regions.

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Seizures induced by three convulsant treatments produced differential effects on the concentration of acetylcholine in rat brain. Status epilepticus induced by (i) coadministration of lithium and pilocarpine caused massive increases in the concentration of acetylcholine in the cerebral cortex and

Evidence for increased activity of mouse brain fatty acid cyclooxygenase following drug-induced convulsions.

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Enzymatic production of prostaglandins (PGs) from exogenous arachidonic acid was studied in brain microsomal fractions prepared from mice following pentylenetetrazol (PTZ)-induced convulsions. Prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) measured either by radioimmunoassay or

Brain levels of N-acylethanolamine phospholipids in mice during pentylenetetrazol-induced seizure.

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The N-acylethanolamine phospholipids (NAPE) are precursors for N-acylethanolamines (NAE), including anandamide (20:4-NAE), which is a ligand for the cannabinoid receptors. Previously, NAPE were believed to be found only in injured tissue, e.g., after neurodegenerative insults. Neuronal injury may

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

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

Regulation of intracellular calcium levels by polyunsaturated fatty acids, arachidonic acid and docosahexaenoic acid, in astrocytes: possible involvement of phospholipase A2.

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Pathological conditions in the brain, such as ischemia, trauma and seizure are accompanied by increased levels of free n-6 and n-3 polyunsaturated fatty acids (PUFA), mainly arachidonic acid (AA, 20:4n-6) and docosahexaenoic acid (DHA, 22:6n-3). A neuroprotective role has been suggested for PUFA.

Molecular Determinants of the Sensitivity to Gq/11-Phospholipase C-dependent Gating, Gd3+ Potentiation, and Ca2+ Permeability in the Transient Receptor Potential Canonical Type 5 (TRPC5) Channel.

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Transient receptor potential canonical type 5 (TRPC5) is a Ca2+-permeable cation channel that is highly expressed in the brain and is implicated in motor coordination, innate fear behavior, and seizure genesis. The channel is activated by a signal downstream of the G-protein-coupled receptor

Modulation of DL-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/quisqualate receptors by phospholipase A2: a necessary step in long-term potentiation?

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The effects of kainate (KA)-induced epileptic seizures on the binding properties of hippocampal glutamate receptors, on the modulation of DL-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/quisqualate receptor by phospholipase A2 (PLA2), and on the formation of long-term potentiation

Human secretory phospholipase A(2), group IB in normal eyes and in eye diseases.

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OBJECTIVE Secretory phospholipases A(2) (sPLA(2)) are enzymes involved in lipid turnover. We recently identified sPLA(2) group IB (GIB) in the rat retina as well as in cerebral neurons and found upregulation to occur in response to light damage and seizures, respectively. The purpose of the present

Quisqualic acid-induced seizures during development: a behavioral and EEG study.

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Quisqualic acid (QA) is an excitatory amino acid analogue that binds to the glutamate ionotropic receptor subclass AMPA (alpha-amino-3 hydroxy-5 methyl-4 isoxazol propionic acid) and metabotropic receptor phospholipase C. To study its epileptogenic properties, we administered QA through an

Secretory phospholipase A2 potentiates glutamate-induced rat striatal neuronal cell death in vivo.

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The secretory phospholipases A2 (sPLA2) OS2 (10, 20 and 50 pmol) or OS1, (50 pmol) purified from taipan snake Oxyuranus scutellatus scutellatus venom, and the excitatory amino acid glutamate (Glu) (2.5 and 5.0 micromol) were injected into the right striatum of male Wistar rats. Injection of 10 and

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