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arachidonic acid/seizures
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Sida 1 från 107 resultat
Involvement of the arachidonic acid cascade in the hypersusceptibility to pentylenetetrazole-induced seizure during diazepam withdrawal.
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The present study was designed to clarify whether the arachidonic acid cascade contributes to the decreased threshold for pentylenetetrazole-induced seizure under benzodiazepine withdrawal in mice. The seizure threshold for pentylenetetrazole was significantly decreased by the discontinuation of
Arachidonic acid inhibits transient potassium currents and broadens action potentials during electrographic seizures in hippocampal pyramidal and inhibitory interneurons.
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The transient outward potassium current was studied in outside-out macropatches excised from the soma of CA1 pyramidal neurons and stratum (st.) oriens-alveus inhibitory interneurons in rat hippocampal slices. Arachidonic acid dose dependently decreased the charge transfer associated with the
Arachidonic acid metabolism in seizures.
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Transient modifications in brain free arachidonic acid in experimental animals durng convulsions.
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Inhibition of GABA-gated chloride channel function by arachidonic acid.
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The effects of arachidonic acid and its metabolites on gamma-aminobutyric acid (GABAA) receptor function were determined in rat cerebral cortical synaptoneurosomes. Incubation of synaptoneurosomes with phospholipase A2 decreased muscimol-induced 36Cl- uptake. Arachidonic acid, the major unsaturated
Metabolic, circulatory, and structural alterations in the rat brain induced by sustained pentylenetetrazole seizures.
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Previous studies have demonstrated that bicuculline-induced seizures of 1-2 h in duration lead to structural, metabolic, and circulatory alterations in the rat brain. Such alterations were observed even though cerebral oxygenation seemed adequate. In the present study, we explored whether
The synthesis of prostaglandins and thromboxane in the mouse brain in vivo. Influence of drug induced convulsions, hypoxia and the anticonvulsants trimethadione and diazepam.
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1. The i.v. administration of convulsant doses of penetrazole or picrotoxin induced an increase in PGF2 alpha, PGE2 and TXB2-like immunoreactive material in mouse brain tissue. The onset of increase coincided with the appearance of clonic seizures. 2. The anticonvulsant drugs trimethadione and
Modification of convulsive behaviour and body temperature in mice by intracerebroventricular administration of prostaglandins, arachidonic acid and the soluble acetylsalicylic acid salt lysine acetylsalicylate.
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The effects of centrally injected prostaglandins (PGE1 and PGF2 alpha), arachidonic acid and lysine acetylsalicylate were examined on the seizure activity and temperature changes produced by pentylentetrazole (PTZ) and also on maximal electroshock (MES) seizures. PGE1 antagonised both PTZ and MES
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
Cyclooxygenase-2/PGE2 pathway facilitates pentylenetetrazol-induced seizures.
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Cyclooxygenases (COXs) are rate-limiting enzymes in the metabolic pathways in which arachidonic acid is converted to prostaglandins. COX-2 is the isoform induced at injury/inflammation sites and expressed constitutively in a few tissues, such as the central nervous system, and plays a role in
Topiramate does not alter expression in rat brain of enzymes of arachidonic acid metabolism.
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BACKGROUND
When administered chronically to rats, drugs that are effective in bipolar disorder-lithium and the anticonvulsants, valproic acid and carbamazepine-have been shown to downregulate the expression of certain enzymes involved in brain arachidonic acid (AA) release and cyclooxygenase
Electroconvulsive seizures regulate gene expression of distinct neurotrophic signaling pathways.
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Electroconvulsive therapy (ECT) remains the treatment of choice for drug-resistant patients with depressive disorders, yet the mechanism for its efficacy remains unknown. Gene transcription changes were measured in the frontal cortex and hippocampus of rats subjected to sham seizures or to 1 or 10
Neuromodulatory role of endogenous interleukin-1β in acute seizures: possible contribution of cyclooxygenase-2.
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The function of endogenous interleukin-1β (IL-1β) signaling in acute seizure activity was examined using transgenic mice harboring targeted deletions in the genes for either IL-1β (Il1b) or its signaling receptor (Il1r1). Acute epileptic seizure activity was modeled using two mechanistically
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.
Chronic lithium administration potentiates brain arachidonic acid signaling at rest and during cholinergic activation in awake rats.
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Studies were performed to determine if the reported 'proconvulsant' action of lithium in rats given cholinergic drugs is related to receptor-initiated phospholipase A2 signaling via arachidonic acid. Regional brain incorporation coefficients k* of intravenously injected [1-14C]arachidonic acid,
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