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An examination of the role of gamma-aminobutyric acid (GABA) in hyperbaric oxygen-induced convulsions in the rat. I. Effects of increased gamma-aminobutyric acid and protective agents.

J L Alderman, Bruce W. Culver, M. Kent Shellenberger

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Abstract

Two approaches have been taken toward testing the hypothesis that a decline in γ-aminobutyric acid (GABA) causes convulsions in animals exposed to high pressure oxygen (OHP). The first was to increase GABA levels by pretreatment with hydrazinopropionic acid (HPA) in doses of 3, 12 and 25 mg/kg or aminooxyacetic acid (AOAA). 25 mg/kg. The second was to pretreat with pentobarbital (38 mg/kg) or disulfiram (200 mg/kg), thereby preventing convulsions. All animals were subsequently exposed to 100% 02 for 90 minutes at 5 atmospheres absolute (60 psig). HPA-and AOAA-induced increases in GABA, ranging from 9 to 2O9% of OHP-exposed saline controls, were accompanied by a shortening of the time to onset and an increase in the frequency and intensity of convulsions. It was concluded that alterations in GABA levels are not causally related to OHP-induced convulsions or to protection from OHP toxicity.

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What this paper is about

Two approaches have been taken toward testing the hypothesis that a decline in γ-aminobutyric acid (GABA) causes convulsions in animals exposed to high pressure oxygen (OHP). The first was to increase GABA levels by pretreatment with hydrazinopropionic acid (HPA) in doses of 3, 12 and 25 mg/kg or aminooxyacetic acid (AOAA). 25 mg/kg. The second was to pretreat with pentobarbital (38 mg/kg) or disulfiram (200 mg/kg), thereby preventing convulsions. All animals were subsequently exposed to 100% 02 for 90 minutes at 5 atmospheres absolute (60 psig). HPA-and AOAA-induced increases in GABA, ranging from 9 to 2O9% of OHP-exposed saline controls, were accompanied by a shortening of the time to onset and an increase in the frequency and intensity of convulsions. It was concluded that alterations in GABA levels are not causally related to OHP-induced convulsions or to protection from OHP toxicity.

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Available abstract

Two approaches have been taken toward testing the hypothesis that a decline in γ-aminobutyric acid (GABA) causes convulsions in animals exposed to high pressure oxygen (OHP). The first was to increase GABA levels by pretreatment with hydrazinopropionic acid (HPA) in doses of 3, 12 and 25 mg/kg or aminooxyacetic acid (AOAA). 25 mg/kg. The second was to pretreat with pentobarbital (38 mg/kg) or disulfiram (200 mg/kg), thereby preventing convulsions. All animals were subsequently exposed to 100% 02 for 90 minutes at 5 atmospheres absolute (60 psig). HPA-and AOAA-induced increases in GABA, ranging from 9 to 2O9% of OHP-exposed saline controls, were accompanied by a shortening of the time to onset and an increase in the frequency and intensity of convulsions. It was concluded that alterations in GABA levels are not causally related to OHP-induced convulsions or to protection from OHP toxicity.

Key concepts: Aminooxyacetic acid, Pentobarbital, Aminobutyric acid, Chemistry, Saline, Disulfiram, Hyperbaric oxygen, Pharmacology

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An examination of the role of gamma-aminobutyric acid (GABA) in hyperbaric oxygen-induced convulsions in the rat. I. Effects of increased gamma-aminobutyric acid and protective agents. — Research Paper | ScholarLens