Interactions between opioid peptides and adrenaline-containing neurons modulate luteinizing hormone secretion in male...

Abstract There is increasing evidence that the opioid inhibition of luteinizing hormone (LH) secretion is mediated, at least in part, by catecholaminergic mechanisms. This study determined the effects of selective manipulation of noradrenergic and adrenergic systems on the ability of opiate receptor blockade to induce the release of LH in adult male rats. Selective depletion of hypothalamic noradrenaline levels by 80% following 6-hydroxydopamine infusions into the central tegmental tract did not alter the 2- to 3-fold increase in serum LH levels following opiate receptor blockade with naloxone (2.5 mg/kg). In contrast, both selective depletion of hypothalamic adrenaline by prior treatment with the phenylethanolamine N-methyltransferase inhibitor, LY134046 (2 x 50 mg/kg) and non-selective depletion of all three catecholamines with alpha-methyl-p-tyrosine (250 mg/kg), abolished the naloxone-induced increase in LH. These results suggest that the inhibition of LH secretion by endogenous opioid peptides is influenced by catecholaminergic neurotransmission and further support the view that adrenaline rather than noradrenaline or dopamine is of importance in this context.