β‐Alanine transport in synaptic plasma membrane vesicles from rat brain

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Abstract
The efflux and exchange of .beta.-alanine were studied in synaptic plasma membrane vesicles from rat brain. The mechanism of .beta.-alanine translocation has been probed by comparing the ion dependence of net efflux to that of exchange. Dilution-induced efflux requires the simultaneous presence of internal sodium and chloride ions while influx is dependent on the presence of these two ions on the outside [Zafra, F., Aragon, M.C., Valdivieso, F. and Gimenez, C. (1984) Neurochem Res. 9, 695-707]. These data show that the release of .beta.-alanine occurs via the carrier system and that it is cotransported with sodium and chloride ions. .beta.-Alanine efflux from the membrane vesicles is stimulated by external .beta.-alanine. This exchange does not require external sodium and chloride but it is dependent on the external concentration of .beta.-alanine. Half-maximal stimulation is obtained at a .beta.-alanine concentration similar to the Km for .beta.-alanine influx. Results of the direct measurements of the coupling of sodium and chloride to the transport of .beta.-alanine by using a kinetic approach allow us to propose a stoichiometry for the translocation cycle catalyzed by the .beta.-alanine transporter of three sodium ions and one chloride ion per .beta.-alanine zwitterion. To account for all the observed effects of external ions, .beta.-alanine concentrations and membrane potential on .beta.-alanine influx and efflux, a kinetic model of the Na+/Cl-/.beta.-alanine cotransport system is discussed.