Sodium-dependent Metabolism and Transport of γ-Aminobutyric Acid in Subcellular Particles from Brain

Abstract

The properties of γ-aminobutyric acid (γABA) are of great interest in the biochemistry and physiology of the vertebrate central nervous system [1]. γABA is found to associate with mitochondria, microsomes and nerve ending particles, all of which can be sedimented from mouse brain homogenates in 0.25 M sucrose by centrifugation between 1,500 and 15,000 × g. When a pellet is resuspended in 0.2 M NaCl (buffered at pH 7.3) and incubated at 0–4° C in the presence of 2-¹⁴C-γABA, a rapid accumulation of radioactivity in the particle occurs. This accumulation is dependent on the presence of Na⁺ ions. A series of studies, reviewed in the preceding paper [2], has led to the postulation of an equilibrating carrier mechanism for the uptake of γABA at 0°C. The Na-dependence of this mechanism lies in a Na⁺ ion requirement for the carrier to bind γABA.

This work was supported in parts by grant NB-01615 from the National Institute of Neurological Diseases and Blindness, National Institutes of Health; grants from the Max C. Fleischmann Foundation and the National Association for Mental Health. The presentation of this work was made possible through funds from grant NB-04270-03 from the National Institute of Neurological Diseases and Blindness, National Institutes of Health.