Interactions of Di‐n‐Propylacetate, Gabaculine, and Aminooxyacetic Acid: Anticonvulsant Activity and the γ‐Aminobutyrate System

Wood, J. D.; Kurylo, E.; Tsui, Sik-Hon

doi:10.1111/j.1471-4159.1981.tb06313.x

Cited by 41 publications

(5 citation statements)

References 24 publications

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“…Using the approach of suicide substrate inhibition or site-directed inhibition, Lippert et al (1977) managed to synthesize a powerful inhibitor of GABA-T without effect on GAD, γ-vinyl GABA, which was subsequently developed into the antiepileptic drug vigabatrin (Rowley et al, 2012). This is compatible with the previous findings of an increased synaptosomal GABA content after treatment with vigabatrin or other inhibitors of GABA-T (Iadarola and Gale, 1980;Wood et al, 1981). This is compatible with the previous findings of an increased synaptosomal GABA content after treatment with vigabatrin or other inhibitors of GABA-T (Iadarola and Gale, 1980;Wood et al, 1981).…”

Section: Gaba Metabolism and Homeostasissupporting

confidence: 63%

Astroglia and Brain Metabolism: Focus on Energy and Neurotransmitter Amino Acid Homeostasis

Schousboe¹,

Walls²,

Bak³

et al. 2015

Colloquium Series on Neuroglia in Biology and Medicine: From Physiology to Disease

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Section: Gaba Metabolism and Homeostasissupporting

confidence: 63%

Astroglia and Brain Metabolism: Focus on Energy and Neurotransmitter Amino Acid Homeostasis

Schousboe¹,

Walls²,

Bak³

et al. 2015

Colloquium Series on Neuroglia in Biology and Medicine: From Physiology to Disease

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“…tent was much less %an that induced by the potent GABA-T inhibitors (Sarhan and Seiler, 1979;Wood et al, 1980Wood et al, , 1981. Surprisingly, however, this increase in GABA level was not accompanied by any concomitant decrease in glutamate content.…”

Section: Gabaculinementioning

confidence: 80%

Changes in the Amino Acid Content of Nerve Endings (Synaptosomes) Induced by Drugs that Alter the Metabolism of Glutamate and γ‐Aminobutyric Acid

Geddes

Wood

1984

Journal of Neurochemistry

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128

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The study was centered on the changes in the amino acid content of nerve endings (synaptosomes) induced by drugs that alter the metabolism of glutamate or gamma-aminobutyric acid (GABA), and that possess convulsant or anticonvulsant properties. The onset of seizures induced by various convulsant agents was associated with a decreased content of GABA and an increased content of glutamate in synaptosomes. The concurrent administration of pyridoxine prevented both the biochemical changes and the convulsions. The administration of gabaculine to mice resulted in large increases in the GABA content of synaptosomes that were counteracted by decreases in glutamate, glutamine, and aspartate levels such that the total content of the four amino acids remained unchanged. The administration of aminooxyacetic acid (0.91 mmol/kg) resulted initially in seizure activity, but subsequently in an anticonvulsant action. No simple relationship existed between the excitable state of the brain induced by aminooxyacetic acid and the changes in the synaptosomal levels of any of the amino acid transmitters. A hypothesis was, however, formulated that explained the convulsant-cum-anticonvulsant action of aminooxyacetic acid on the basis of compartmentation of GABA within the nerve endings.

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“…It has been proposed that some actions of AOAA may involve components which are not associated with GABA neurotransmission (Wood et al 1981;Löscher 1981b;Bernasconi et al 1982). To diffe¬ rentiate the specific GABA-mediated effects from the side-effects we have combined the GABA-T inhibitor with the GABA antagonist bicuculline.…”

Section: Discussionmentioning

confidence: 99%

Effects of increase of brain GABA levels on the hypothalamic-pituitary-luteinizing hormone axis in rats

Donoso¹,

Banzán²

1984

Acta Endocrinologica

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The effects of increasing brain GABA levels by administration of aminooxyacetic acid (AOAA), a GABA-transaminase inhibitor, on tonic and induced LH release were evaluated in ovariectomized rats.Pulsatile LH release was clearly inhibited by AOAA. Mean plasma LH levels fell, the frequently of pulses decreased, and the intervals between pulses increased. An absence of LH pulses was seen in some animals. Administration of the GABA antagonist, bicuculline, prevented these modifications. In addition, it enhanced mean plasma LH levels. AOAA blunted the rise of plasma LH levels produced by either oestradiol or progesterone in oestradiol-primed ovariectomized rats. In contrast, the AOAA treatment apparently facilitated the inhibitory feedback of oestradiol on LH release. The acute release of LH produced by LRH injection was not altered by AOAA.The results support the view that brain GABA exerts an inhibitory action on LH release in the rat.

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Interactions of Di‐n‐Propylacetate, Gabaculine, and Aminooxyacetic Acid: Anticonvulsant Activity and the γ‐Aminobutyrate System

Cited by 41 publications

References 24 publications

Astroglia and Brain Metabolism: Focus on Energy and Neurotransmitter Amino Acid Homeostasis

Astroglia and Brain Metabolism: Focus on Energy and Neurotransmitter Amino Acid Homeostasis

Changes in the Amino Acid Content of Nerve Endings (Synaptosomes) Induced by Drugs that Alter the Metabolism of Glutamate and γ‐Aminobutyric Acid

Effects of increase of brain GABA levels on the hypothalamic-pituitary-luteinizing hormone axis in rats

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