Exp Brain Res 1987 ;66(2):378-84
Previous circumstantial evidence suggested that endogenous opioid peptides inhibit an excitatory noradrenergic projection to the medial preoptic area (MPOA), and thereby suppress the activity of neurones containing luteinising hormone-releasing hormone and thus systemic concentrations of luteinising hormone (LH) itself. In this paper, we report that electrically stimulated release of 3H-Noradrenaline (3H-NA) from perifused slices of rat MPOA is diminished when opioid agonists are added to the incubation medium. Thus, morphine (10 microM), beta-Endorphin (1 microM) and met-Enkephalin (1 microM), but not Dynorphin A (1-8) (1 microM), caused a significant decrease in electrically stimulated 3H-NA release. The inhibition was reversed by addition of naloxone (10 microM) to the perifusion medium but 3H-NA release was unaffected by dopamine or acetylcholine (or their antagonists sulpiride and atropine, respectively), or serotonin, neurotensin, muscimol or bicuculline (the latter two being agonist and antagonist respectively for the GABA A receptor). Therefore, the experiments provide direct evidence that brain opioids modulate the noradrenergic input to MPOA neurones and support the hypothesis that this may be one mechanism for the regulation of LH secretion.