Bromocriptine-induced inhibition of plasma dopamine, noradrenaline and adrenaline responses to LH-RF

Abstract

IN addition to their regulatory role on pituitary hormones, hypothalamic-hypophyseal regulatory hormones may function in brain as neurotransmitters. Thus, in addition to the considerable evidence in laboratory animals suggesting that the release of luteinising hormone releasing factor (LH-RF) is regulated by brain amines¹, further evidence suggests that LH-RF may function at central nervous system synapses. It is found within synaptosomes and vesicle-like structures in various areas of brain²; it influences animal behaviour through a direct action in brain³, and microiontophoretic applications of LH-RF to neurones in the mediobasal hypothalamus and preoptic area are associated with prominent short-term changes in neuronal excitability, the most frequently observed effect being decreased excitability⁴. It has been suggested that axon collaterals within a putative peptidergic neuronal network may function in feedback circuits regulating activity of the tuberoinfundibular system and to inform other brain regions about the activity of this system. It seems reasonable to speculate that LH-RF release from such peptidergic neurones may act as a neurotransmitter or modulator to regulate the activity of certain central aminergic neurones. Thus, we examined the effects of LH-RF on plasma catecholamines in normal men, and found a rapid decrease in plasma concentrations of dopamine, noradrenaline and adrenaline (Fig. 1). Furthermore, bromocriptine, a dopamine receptor agonist, entirely prevented this depressant effect of LH-RF on plasma catecholamines.