Role of sodium in neuronal uptake of monoamines and amino acid precursors

Abstract

IT is generally accepted that the neuronal re-uptake of monoaminergic neurotransmitters after their release into the synaptic cleft, inactivates transmitter action^1,2. The amino acid precursors L-tyrosine and L-tryptophan are also taken up by neurones from the circulation^3–5. Using in vitro models of these processes, it has been demonstrated that tricyclic anti-depressant drugs inhibit the uptake of both the amines^6,7 and their precursors⁸ into synaptosomal fractions obtained from rat brain homogenates. Amino acids can be transported into cells by an Na⁺-dependent, Na⁺-independent or an Na⁺-inhibited transport system⁹. Monoamines, however, have been reported^10,11 to have only an Na⁺-dependent system. Since information is lacking concerning the uptake of L-tyrosine and L-tryptophan, we have attempted to determine the role of Na⁺ ions in the uptake of the amino acid precursors compared with that of monoamines.