, Volume 10, Issue 5, pp 447-462

The inactivation of extracellularly administered amino acids in the feline spinal cord

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The mercurials, p-hydroxymercuribenzoate and p-chloromercuriphenylsulphonate, administered electrophoretically from multi-barelled micropipettes, potentiate the depressant action of similarly administered glycine on feline spinal neurones. In addition, these mercurials inhibit the transport of glycine into rat brain slices. Neither action is very specific for glycine, since slightly higher concentrations of p-chloromercuriphenylsulphonate than those required to potentiate glycine-induced depression also potentiate depression induced by GABA, β-alanine, Land D-α-alanine, and even higher concentrations enhance the excitant action of acidic amino acids. p-Hydroxymercuribenzoate also inhibits the uptake of GABA, DL-aspartate and L-lysine by brain slices. The potentiation by the mercurials of amino acid-induced effects is considered likely to be the result of inhibition of transport processes rather than enzymic activities.

Thiosemicarbazide, administered electrophoretically and intravenously, does not enhance the effects of amino acid excitants or depressants on spinal interneurones. Hydrazinopropionic acid, a potent inhibitor of GABA transaminase, does not enhance GABA-induced depression of spinal interneurones when administered electrophoretically.

These findings suggest the importance of transport processes in the removal of amino acids from the synaptic environment, and evidence is discussed that these processes are likely to differ in detail from the observed gross transport of amino acids into tissue slices.