STUDIES OF THE UPTAKE AND RELEASE OF [3H]β‐ALANINE BY FROG SPINAL SLICES

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Abstract
Abstract— [3H]β‐Alanine was accumulated by frog spinal cord slices by two transport components with estimated Km values of 31 M (‘high‐affinity’) and 11 HIM (‘low affinity’) respectively. The high affinity uptake exhibited sodium ion and energy dependence, temperature sensitivity, had a very low Vmax (10.4 nmol/g/min) compared to GABA and glycine, was competitively inhibited by GABA (Kt 2 M), and was significantly reduced by the presence of glycine and of taurine in the incubating medium.When slices preloaded with [3H]β‐alanine were superfused with medium containing depolarizing concentrations of potassium ions, there was a small, but consistent, increase in [3H]β‐alanine efflux: 1.4 times prestimulation rates in 40 mM potassium. When the superfusate was altered by omission of calcium and addition of concentrations of magnesium (10 mm), manganese (1 mM), and cobalt (1 mM) ions sufficient to block reflex transmission in the isolated in vitro frog cord, the potassium‐evoked release was not blocked. Release was decreased by lanthanum ions (1 mM). Release of [3H]GABA and [3H]glycine in parallel experiments was inhibited by magnesium, manganese, cobalt and lanthanum. Veratridine significantly increased the release of [3H]GABA and [3H]glycine but not of [3H]β‐alanine.These observations demonstrate the non‐specificity of β‐alanine uptake and the unconventional nature of the calcium‐dependence of β‐alanine release and therefore do not lend support to the hypothesis that β‐alanine functions as a neurotransmitter in frog spinal cord.