Sequential Lowering and Raising of Brain γ-Aminobutyric Acid Levels by Isonicotinic Acid Hydrazide

1971 ◽  
Vol 49 (8) ◽  
pp. 780-781 ◽  
Author(s):  
J. D. Wood ◽  
S. J. Peesker

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 was followed by a reversal of the effect such that the GABA level became greater than that in untreated control chicks.

1972 ◽  
Vol 50 (12) ◽  
pp. 1217-1218 ◽  
Author(s):  
J. D. Wood ◽  
S. J. Peesker ◽  
J. I. M. Urton

The administration of isonicotinic acid hydrazide (2.2 mmol/kg) plus pyridoxine (4.4 mmol/kg) to chicks 14–18 h prior to exposure to hyperbaric oxygen provided excellent protection against the onset of oxygen-induced seizures in the birds.


1973 ◽  
Vol 51 (12) ◽  
pp. 959-965 ◽  
Author(s):  
J. D. Wood ◽  
S. J. Peesker

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-induced seizures in the birds. The hydrazide was the active anticonvulsant component of the drug mixture but pyridoxine was necessary to prevent seizures induced by the hydrazide itself shortly after its administration. The anticonvulsant action of the drug mixture developed relatively slowly but lasted for several hours and correlated well with concomitant changes in the concentration of γ-aminobutyric acid (GABA) in the brain. No similar correlation was observed between the anticonvulsant action and the activity of either glutamic acid decarboxylase or GABA-α-oxoglutarate aminotransferase.


PEDIATRICS ◽  
1992 ◽  
Vol 90 (2) ◽  
pp. 221-223
Author(s):  
STEVEN B. COKER

Vitamin B6 acts as coenzyme in decarboxylation and transamination of amino acids. Pyridoxal phosphate is the coenzyme for a glutamic decarboxylase and γ-aminobutyric acid transaminase, enzymes necessary in production and metabolism of brain γ-aminobutyric acid. Vitamin B6 deficiency has been known to produce peripheral neuritis, dermatitis, anemia, and convulsions in infants.1 Administration of isonicotinic acid hydrazide may produce a vitamin B6-responsive neuropathy. Convulsions from vitamin B6 dependency occur despite normal vitamin B6 levels. These seizures, according to pediatric and neurological texts, occur immediately after birth up to 6 months.1-4 In 1985, Goutieres and Aicardi5 described three patients with atypical pyridoxine-dependent seizures with onset at 7 weeks, 5 days, and 4 months.


1954 ◽  
Vol 209 (2) ◽  
pp. 467-484 ◽  
Author(s):  
Leonard J. Zatman ◽  
Nathan O. Kaplan ◽  
Sidney P. Colowick ◽  
Margaret M. Ciotti

2011 ◽  
Vol 4 (3) ◽  
pp. 211-217 ◽  
Author(s):  
Asha B. Thomas ◽  
Piyoosh A. Sharma ◽  
Preeti N. Tupe ◽  
Ravindra V. Badhe ◽  
Rabindra K. Nanda ◽  
...  

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