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DEVELOPMENT OF AN EXPRESSION WHICH RELATES THE EXCITABLE STATE OF THE BRAIN TO THE LEVEL OF GAD ACTIVITY AND GABA CONTENT, WITH PARTICULAR REFERENCE TO THE ACTION OF HYDRAZINE AND ITS DERIVATIVES
TLDR
The results together with previous data obtained were used to develop an equation which related the excitable state of the brain to changes in overall GABA metabolism, and it was suggested that the values obtained might reflect the content of GABA in a critical subcellular location such as the synaptic cleft. Expand
THE ANTICONVULSANT ACTION OF GABA‐ELEVATING AGENTS: A RE‐EVALUATION
TLDR
Aminooxyacetic acid was the most efficacious in delaying drug‐induced seizures in mice whereas hydroxylamine brought about only a slight delay in the onset of seizures. Expand
THE ROLE OF GABA METABOLISM IN THE CONVULSANT AND ANTICONVULSANT ACTIONS OF AMINOOXYACETIC ACID
TLDR
The state of excitability of the brain following the administration of AOAA was related, within the limits of the present study, to changes in GAD activity and GABA levels, but additional data are required before the relationship can be properly evaluated. Expand
THE EFFECT ON GABA METABOLISM IN BRAIN OF ISONICOTINIC ACID HYDRAZIDE AND PYRIDOXINE AS A FUNCTION OF TIME AFTER ADMINISTRATION
TLDR
The administration of pyridoxine together with the INH prevented the onset of seizures and lessened the effect of the InH on GABA levels and GAD activity but not on GABA‐T activity, suggesting the possibility that a deranged GABA metabolism is responsible for hydrazide‐induced seizures. Expand
A correlation between changes in GABA metabolism and isonicotinic acid hydrazide-induced seizures.
TLDR
The intramuscular administration of INH to chicks caused striking changes in brain GABA metabolism during a 16 h period following the injection and seizure activity in the chicks did bear a relationship to a function which incorporated changes in both GABA levels and GAD activity. Expand
Sequential lowering and raising of brain gamma-aminobutyric acid levels by isonicotinic acid hydrazide.
  • J. Wood, S. J. Peesker
  • Chemistry, Medicine
  • Canadian journal of physiology and pharmacology
  • 1 August 1971
The intramuscular administration of isonicotinic acid hydrazide to chicks produced initially a rapid and significant decrease in the concentration of brain γ-aminobutyric acid (GABA) which wasExpand
Effect of L-cycloserine on brain GABA metabolism.
TLDR
The prior administration of L-cycloserine to mice significantly delayed the onset of isonicotinic acid hydrazide induced convulsions and L-Cycloserine was also a potent in vitro inhibitor of brain GABA-T activity. Expand
The anticonvulsant properties of isonicotinic acid hydrazide and associated changes in gamma-aminobutyric acid metabolism.
  • J. Wood, S. J. Peesker
  • Chemistry, Medicine
  • Canadian journal of physiology and pharmacology
  • 1 December 1973
The administration of isonicotinic acid hydrazide and pyridoxine to chicks prior to their being exposed to oxygen at high pressure brought about a delay in the onset of the hyperbaric-oxygen-inducedExpand
A dual mechanism for the anticonvulsant action of aminooxyacetic acid.
  • J. Wood, S. J. Peesker
  • Chemistry, Medicine
  • Canadian journal of physiology and pharmacology
  • 1 August 1976
TLDR
The intramuscular injection of aminooxyacetic acid into mice elevated the concentration of gamma-aminobutyric acid in the brain, inhibited glutamic acid decarboxylase activity and delayed the onset of isonicotinic acid hydrazide induced seizures, indicating that the anticonvulsant action of AOAA involved two mechanisms. Expand
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