KINETICS OF BRAIN GLUTAMATE DECARBOXYLASE. INHIBITION STUDIES WITH N‐(5′‐PHOSPHOPYRIDOXYL) AMINO ACIDS 1

@article{Bayn1977KINETICSOB,
  title={KINETICS OF BRAIN GLUTAMATE DECARBOXYLASE. INHIBITION STUDIES WITH N‐(5′‐PHOSPHOPYRIDOXYL) AMINO ACIDS 1},
  author={Alejandro Bay{\'o}n and Lourival Domingos Possani and Ricardo Tapia},
  journal={Journal of Neurochemistry},
  year={1977},
  volume={29}
}
Abstract— Seven N‐(5′‐phosphopyridoxyl) amino acids, reduced analogs of the glutamate‐pyridoxal phosphate Schiff base, were synthesized and purified. All of them inhibited mouse brain glutamate decarboxylase activity. The four most potent inhibitors were the aminooxyacetate, GABA, cysteinesul‐finate and glutamate derivatives, and the effect of these compounds was studied kinetically. The inhibition produced was in all cases mixed function with respect to glutamate and competitive with respect… 
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TLDR
Computer simulations of this model reproduced all the observed features of the enzyme behavior and showed that the free pyridoxal phosphate‐dependent activity can be abolished when either all substrate or all cofactor are in the form of Schiff base.
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TLDR
The interaction of glutamate decarboxylase with its cofactor, pyridoxal 5′-phosphate, is a regulated process and appears to be one of the major means of controlling enzyme activity.
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TLDR
It is suggested that zinc may play a role in pyridoxal phosphate-mediated regulation of glutamic acid decarboxylase, a major inhibitory neurotransmitter in the CNS.
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The binding of GAD to negatively charged liposomes is primarily ionic, and the GAD molecules that bind to the liposome seem to be deficient in free PLP and therefore, are probably more susceptible to regulation by the coenzyme.
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TLDR
The results indicate that the susceptibility of GAD in vivo to a diminished cofactor concentration decreases with age, and it seems possible that changes in the expression of enzyme forms are reflected in developmental variations in the susceptibility to seizures induced by vitamin B6 depletion, but alterations of other B6-dependent biochemical pathways cannot be discarded.
Pyridoxal phosphate-unrelated inhibition of hippocampal glutamic acid decarboxylase by convulsant pyridoxal sulphate
TLDR
The inhibition was demonstrated, whether glutamic acid decarboxylase was assayed in the presence or absence of its coenzyme pyridoxal phosphate, and the activity of glutic-clonic convulsions in other brain regions was unaffected following chronic application of pyrdoxal sulphate.
The selective inhibition of hippocampal glutamic acid decarboxylase in zinc-induced epileptic seizures
TLDR
The intracerebroventricular administration of Zn2+ causes epileptic seizures characterized by running fits, jumping, vocalization, fasiculation of facial muscles, myoclonic movements of the limbs and tonic-clonic convulsions and the inhibition of glutamic acid decarboxylase by Zn1+ was selective occurring only in hippocampus and not in the hypothalamus, amygdala, caudate or thalamus.
Regulation and function of pyridoxal phosphate in CNS
  • M. Ebadi
  • Medicine, Chemistry
    Neurochemistry International
  • 1981
TLDR
By understanding the factors that regulate the synthesis, binding, storage and degradation of pyridoxal phosphate in the brain, a better insight into the role of vitamin B(6) in neurobiology may be gained.
CHAPTER 22 – REGULATION AND FUNCTION OF PYRIDOXAL PHOSPHATE IN CNS
Pyridoxal phosphate and pyridoxamine phosphate, the catalytically active forms of vitamin B6, influence brain function by participating at stages in metabolism of proteins, lipids, carbohydrates,
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The kinetics of the inhibition of mouse brain glutamate decarboxylase by pyri‐doxaI‐5′‐phosphate oxime‐O‐acetic acid (PLPOAA) was studied. The inhibition was noncompetitive with regard to glutamic
KINETICS OF BRAIN GLUTAMATE DECARBOXYLASE. INTERACTIONS WITH GLUTAMATE, PYRIDOXAL 5‐PHOSPHATE AND GLUTAMATE‐PYRIDOXAL 5‐PHOSPHATE SCHIFF BASE 1
TLDR
Computer simulations of this model reproduced all the observed features of the enzyme behavior and showed that the free pyridoxal phosphate‐dependent activity can be abolished when either all substrate or all cofactor are in the form of Schiff base.
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TLDR
Some relationships between the level of pyridoxal phosphate in brain and the characteristic periods of convulsions induced by 1,1-dimethylhydrazine (UDMH) are reported and evidence is presented which indicates that once the initial convulsion has occurred, the timing of the succeeding ones is controlled byamechanism that does not involve detectable changes in the level.
Evidence for a role of glutamate decarboxylase activity as a regulatory mechanism of cerebral excitability
TLDR
The results suggest that under normal conditions GABA is not being released from a storage pool specifically related to i ts synaptic function, but, instead, that the newly synthesized GABA is being liberated into the synaptic cleft (TAPIA, 1974).
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symposia was held in October 1974 in New Delhi and considered growth and development of the brain, and the prcceedings are now presented under the editorship ef Dr. Mary Brazier. Contributions
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