Inactivation of the convulsant site of the GABA(A) receptor complex by arginine-specific reagents and its protection by the anion binding sites

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Abstract

1 [35S]t-Butylbicyclophosphorothionate (TBPS) binding to the convulsant sites of the γ-aminobutyric acid (GABA(A)) receptor complex was measured in washed membranes prepared from rat forebrain. 2 A concentration-dependent decrease in TBPS binding was observed with pretreatment by arginine-selective reagents in the following order of potency: p-chloro-phenylglyoxal > phenylglyoxal > 2,3-butanedione > 1,2-cyclohexanedione > camphorquinone-10-sulphonic acid. 3 Inactivation by butanedione pretreatment was attenuated by sodium salts of the Eccles anions chloride and bromide. Tartarate and sulphate salts were ineffective. 4 The decrease in TBPS binding by butanedione pretreatment could not be prevented by GABA or by picrotoxinin, a ligand of the convulsant sites. 5 Pretreatment of the membranes at 30°C with sodium bromide resulted in a concentration-dependent increase in TBPS binding (EC50=63 mM). 6 The submaximally enhancing effect of 250 mM sodium bromide was amplified by GABA and attenuated by the GABA(A) antagonist SR 95531. 7 It is concluded that arginine residues might participate in the binding of Eccles anions at the mouths of the GABA(A)-chloride ionophores.

Original languageEnglish
Pages (from-to)161-165
Number of pages5
JournalMolecular Neuropharmacology
Volume3
Issue number3
Publication statusPublished - Jan 1 1993

ASJC Scopus subject areas

  • Neuroscience(all)
  • Pharmacology

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