Dextro‐phenylalanine inhibits potassium‐evoked 3H‐noradrenaline release from hypothalamus but not of 3H‐dopamine from rat caudate nucleus

Abstract

Action of dextro‐phenylalanine (d‐Phe) on catecholamine release elicited by K⁺ 20 mM has been studied in isolated slices of rat central nervous system (CNS). d‐Phe (3 × 10⁻³ M) produced inhibition of the fractional release of ³H‐noradrenaline but not of ³H‐dopamine. The mentioned effect is Ca²⁺ dependent and was antagonized when this ion was incremented to 2.6 mM in the medium or in the presence of ionophore A‐23187 (4 × 10⁻⁵ M). Neither acetylsalicylic acid nor indomethacin (prostaglandin biosynthesis inhibitors) interferes with the effect of d‐Phe, showing that by itself it would not reach through the prostaglandin pathway. d‐Phe modified neither the noradrenaline neuronal uptake nor its metabolism at the CNS. The findings suggest that d‐Phe acts through a Ca²⁺‐dependent mechanism, possibly by specific receptors and in parallel with feedback circuits that involve alpha‐adrenoceptors, muscarinic receptors, or prostaglandins.