gamma aminobutyric acid/seizures

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Release of gamma-aminobutyric acid from isolated brain synaptosomes during semicarbazide-induced convulsions.

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The in vivo effect of semicarbazide (SC) and aminoxyacetic acid (AOAA) upon gamma-aminobutyric acid (GABA) levels in the synaptosomal fraction, and GABA release from the same fraction were studied in the mouse. The convulsive dose of SC reduced the GABA content in synaptosomes, and when the

Relationship between gamma-aminobutyric acid metabolism and antivitamin B6-induced convulsions.

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The correlation between the gamma-aminobutyric acid (GABA) metabolism and convulsions by some vitamin B6 antagonists, DL-penicillamine (PeA), hydrazine (Hyd), thiosemicarbazide (TSC) were investigated. Glutamic acid decarboxylase (GAD) and gamma-aminobutyric acid transaminase (GABA-T) activities

Synergistic effect of phosphatidylserine with gamma-aminobutyric acid in antagonizing the isoniazid-induced convulsions in mice.

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The influence of phosphatidylserine (PS) on the isoniazid-induced convulsions has been studied in mice. Sonicated dispersions of this phospholipid given intravenously do not show anticonvulsant activity but they do so when gamma-aminobutyric acid (GABA) is simultaneously injected. GABA alone is

Evidence for an involvement of nitric oxide and gamma aminobutyric acid in the anticonvulsant action of L-arginine on picrotoxin-induced convulsions in rats.

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Five, 30, and 60 min pretreatment of 1000 mg/kg and not 500 mg/kg of L-arginine inhibited convulsions induced by picrotoxin. The concentrations of nitric oxide (NO) and gamma aminobutyric acid (GABA) were increased in the brain 5, 30, and 60 min after administration of 1000 mg/kg and not 500 mg/kg

Absence of modifications in gamma-aminobutyric acid metabolism after repeated generalized seizures in amygdala-kindled rats.

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Alterations in gamma-aminobutyric acid (GABA) metabolism have been investigated in the kindling model of epilepsy. Numerous generalized seizures were induced by amygdala-kindling stimulations in rats. One week after the last stimulation, there were no changes in GABA levels nor in the activity of

Study on hyperbaric oxygen-induced convulsion with particular reference to gamma-aminobutyric acid in synaptosomes.

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When mice were exposed to 100% oxygen at a pressure of 6 atm. absolute, the animals suffered from severe convulsions. The content of gamma-aminobutyric acid (GABA) in synaptosomes was lower in the exposed animals than in unexposed ones. The exposure to high pressure oxygen produced a considerable

gamma-Aminobutyric acid metabolism in subcellular particles of mouse brain and its relationship to convulsions.

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The in vivo effects of convulsant drugs (hydrazine and penicillamine) on the metabolism of gamma-aminobutyric acid (GABA) in subcellular fractions of mouse brain were studied. Both substances inhibited the activity of glutamic acid decarboxylase [EC 4.1.1.15] (GAD) in the synaptosomal fraction

Inhibition of acute hyperammonemia-induced convulsions by systemically administered gamma aminobutyric acid in rats.

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The present study has investigated the effects of intraperitoneally administered gamma aminobutyric acid (GABA) on ammonium chloride-induced hyperammonemia and convulsions in rats. Systemically administered GABA did not alter the concentration of GABA in the brain of control as well as

Kindled seizures result in decreased responsiveness of benzodiazepine receptors to gamma-aminobutyric acid (GABA).

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Repeated kindled seizures result in increased numbers of benzodiazepine receptors in fascia dentata membranes. Our previous work localized these receptors to a discrete neuronal population, the dentate granule cells. The present investigation characterizes the regulation of this binding by NaCl,

Ovariectomy aggravates convulsions and hippocampal gamma-aminobutyric acid inhibition induced by cyclosporin A in rats.

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The possible cyclosporin A application for rheumatoid arthritis that develops preferentially in middle-aged women raises concerns about adverse effects of cyclosporin A, including neurotoxicity in patients with climacterium. The present study was aimed at elucidating the effect of cyclosporin A on

Overexpression of gamma-aminobutyric acid transporter subtype I leads to susceptibility to kainic acid-induced seizure in transgenic mice.

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Gamma-aminobutyric acid (GABA) is the principal inhibitory neurotransmitter, and the GABAergic synaptic transmission is normally terminated by the rapid uptake through GABA transporters. With transgenic mice ubiquitously overexpressing GABA transporter subtype I (GAT1), the present study explored

Cerebral glutamic acid decarboxylase activity and gamma-aminobutyric acid concentrations in mice susceptible or resistant to audiogenic seizures.

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DBA/2 mice between 21 and 28 days of age are highly susceptible to sound-induced seizures. Drug studies suggest a possible deficit of gamma-aminobutyric acid (GABA)-mediated neurotransmission may be involved. We have measured the whole brain GABA concentration and glutamic acid decarboxylase

Inhibition by gamma-aminobutyric acid system activation of epileptic seizures in spontaneously epileptic rats.

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The effects of muscimol, a gamma-aminobutyric acid (GABA)A-receptor agonist, and aminooxy-acetic acid (AOAA), an inhibitor of GABA-converting enzyme, on tonic and absence-like seizures in spontaneously epileptic rats (SER: zi/zi, tm/tm) were investigated to elucidate whether GABAergic function

The changes in the expressions of gamma-aminobutyric acid transporters in the gerbil hippocampal complex following spontaneous seizure.

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To identify the roles of gamma-aminobutyric acid (GABA) transporter in epileptogenesis and the recovery mechanisms in spontaneous seizure, a chronological and comparative analysis of GABA transporters (GAT) expression was conducted. GAT-1 immunoreactivity was more strongly detected in the

Gamma-aminobutyric acid concentration in lumbar cerebrospinal fluid from patients with febrile convulsions and controls.

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The cerebrospinal fluid (CSF) concentration of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) was analysed in 41 children with febrile convulsions (FC), 41 febrile controls of similar age (control group 1), and 59 controls, who had no fever and/or were outside the age range for FC

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