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gamma butyrolactone/seizures
Nuoroda įrašoma į mainų sritį
Puslapis 1 nuo 71 rezultatus
Proteomic analysis of gamma-butyrolactone-treated mouse thalamus reveals dysregulated proteins upon absence seizure.
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Absence seizure has been of interest because the symptom is related to sensory processing. However, the mechanism that causes the disease is not understood yet. To better understand the molecular mechanism related to the disease progress at protein level, we performed proteomic studies using the
Effects of gamma-hydroxybutyrate and gamma-butyrolactone derivates on spontaneous generalized non-convulsive seizures in the rat.
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The effects of derivatives of gamma-hydroxybutyrate (GHB) and gamma-butyrolactone were examined in Wistar rats from a strain in which spontaneous spike-and-wave discharges can be recorded electroencephalographically. For each compound, the effects were compared to those obtained in rats from a
The gamma-hydroxybutyrate model of absence seizures: correlation of regional brain levels of gamma-hydroxybutyric acid and gamma-butyrolactone with spike wave discharges.
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gamma-Hydroxybutyric acid (GHB) produces a constellation of EEG and behavioral changes when given to animals, which represent an experimental model of generalized absence seizures. gamma-Butyrolactone (GBL), the prodrug of GHB, produces these changes more rapidly and consistently than GHB, such that
A dissociation of gamma-butyrolactone-induced absence seizure and CRE- and AP-1 DNA-binding activities in the developing rat brain.
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Generalized absence epilepsy is a neurological childhood disorder which is characterized by behavioral arrest with staring and by 3 Hz spike and wave discharges (SWDs) in the electroencephalogram (EEG). In the present study, we investigated the correlation between behavioral and EEG changes and
Pharmacological profiles of absence seizure-induced increases in CRE- and AP-1 DNA-binding activities in gamma-butyrolactone-treated mice.
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Absence seizures are characterised by a well-defined disturbance of thalamocortical function, and there is no spread to other systems. In this study, we continue our examination of the mechanisms underlying the increased nuclear cyclic AMP responsive element (CRE)- and activator protein 1 (AP-1)
gamma-Butyrolactone-induced absence-like seizures increase nuclear CRE- and AP-1 DNA-binding activities in mouse brain.
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We examined the involvement of the GABAB receptor and the coordinated induction of nuclear transcriptional factors in experimental generalized absence seizures induced by gamma-butyrolactone (GBL) in mice. Although administration of GBL 50 mg/kg did not show any effects on behavior or ECoG pattern,
Impact of strain, sex, and estrous cycle on gamma butyrolactone-evoked absence seizures in rats.
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Childhood absence epilepsy (CAE) is the most common pediatric epilepsy syndrome and is characterized by typical absence seizures (AS). AS are non-convulsive epileptic seizures characterized by a sudden loss of awareness and bilaterally generalized synchronous 2.5-4 Hz spike and slow-wave discharges
[The mechanism(s) of alpha-(aminoethyl)-gamma-butyrolactone. In vivo studies in mice].
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This paper describes the synthesis of alpha-(dimethylaminoethyl)-gamma, gamma-diphenyl-gamma-butyrolactone 4. The study of convulsions induced, on mice, by this compound could show the existence of antiGABAergic and cholinergic action components, but, unlike the homologous alpha-
Cerebral hemodynamic responses to seizure in the mouse brain: simultaneous near-infrared spectroscopy-electroencephalography study.
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We applied near-infrared spectroscopy (NIRS) and electroencephalography (EEG) simultaneously on the mouse brain and investigated the hemodynamic response to epileptic episodes under pharmacologically driven seizure. gamma-butyrolactone (GBL) and 4-aminopyridine (4-AP) were applied to induce absence
An investigation of the relationship between the dopaminergic and electroencephalographic effects of gamma-butyrolactone.
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An investigation was made into the relationship between dopaminergic and EEG effects of gamma-butyrolactone (GBL) by comparing time-course and dose-response studies of these two actions of gamma-butyrolactone in rats implanted with permanent cortical electrodes. Dopaminergic effects were assessed by
Noradrenergic mechanisms in gamma-hydroxybutyrate-induced seizure activity.
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The electroencephalographic (EEG) response of 6-hydroxydopamine (6-OHDA)-treated and control rats to gamma-butyrolactone (GBL) the prodrug of gamma-hydroxybutyrate (GHB), was determined. Neonatal treatment with 6-OHDA produced a significant reduction of noradrenaline in cortex and hippocampus while
Enantioselectivity of alpha-benzyl-alpha-methyl-gamma-butyrolactone-mediated modulation of anticonvulsant activity and GABA(A) receptor function.
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Alkyl-substituted butyrolactones have both inhibitory and stimulatory effects on GABA(A) receptors. Lactones with small alkyl substitutions at the alpha-position positively modulate the channel, whereas beta-substituted lactones tend to inhibit the GABA(A) receptor. These compounds mediate
Alkyl-substituted thiolo-, thiono-, and dithio-gamma-butyrolactones: new classes of convulsant and anticonvulsant agents.
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A series of sulfur-containing congeners have been prepared from alpha-ethyl-alpha-methyl-gamma-butyrolactone, beta-ethyl-beta-methyl-gamma-butyrolactone, and alpha,alpha,beta,beta-tetramethyl-gamma-butyrolactone as potential neuropharmacologic agents. The lactones were treated with benzyl mercaptide
Alpha-spirocyclopentyl- and alpha-spirocyclopropyl-gamma-butyrolactones: conformationally constrained derivatives of anticonvulsant and convulsant alpha,alpha-disubstituted gamma-butyrolactones.
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To further study the putative gamma-butyrolactone site of the GABAA/chloride channel complex, constrained derivatives of convulsant and anticonvulsant alpha,alpha-disubstituted gamma-butyrolactones (alpha-spirocyclopropyl- and alpha-spirocyclopentyl-gamma-butyrolactones) were synthesized and
Withdrawal from gamma-hydroxybutyrate, 1,4-butanediol and gamma-butyrolactone: a case report and systematic review.
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1,4-butanediol (1,4-BD) is an industrial solvent that is metabolized to gamma-hydroxybutyrate (GHB), a gamma-aminobutyric acid agonist and central nervous system depressant. GHB and its analogues are popular drugs of abuse. Withdrawal from these agents is characterized by autonomic instability and
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