Cation Dependence of Hypotaurine Uptake in Mouse Brain Slices

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Abstract
Mouse brain slices take up hypotaurine (2-aminoethanesulfinic acid) from medium by means of 2 concentrative low- and high-affinity transport systems. [35S]Hypotaurine uptake by the slices was significantly reduced in the absence of external K+, Ca2+ or Mg. An excess of K inhibited hypotaurine uptake by 1/2. Uptake was almost completely abolished on removal of Na. The Km constants for both low- and high-affinity transport components increased in a low-Na medium, suggesting that Na+ are required when hypotaurine is attached to its possible carrier sites in plasma membranes. Na also mimicked allosteric effectors of hypotaurine transport, showing positive cooperativity. More than 2 Na+ may be involved in the transport of 1 hypotaurine molecule across the cell membrane. The calculated activation energies of transport were fairly similar in normal and Na deficient media and Na+ may not participate in the activation mechanisms of the transport. With respect to cation dependence, hypotaurine transport in brain slices exhibits features characteristic of neurotransmitter amino acids.