Opiate inhibition of peptide release from the neurohumoral terminals of hypothalamic neurones

Abstract

The release of peptides from the magnocellular neurones of the hypothalamus, whose axons terminate on capillaries in the neurohypophysis, has been likened to the release of neuro-transmitters from conventional synapses in other parts of the nervous system¹. These oxytocin and vasopressin producing neurones generate action potentials within their perikarya, and the number and pattern of spikes propagated to the neurohypophysis govern the quantity of peptide released into the circulation^2,3. We do not know, however, if the release of these peptides is modified at the level of the axon terminal as occurs in conventional synapses in the form of presynaptic inhibition or facilitation^4,5. Within the hypothalamo-neurohypophysial system a mechanism of this type could operate either synaptically through the axo-axonal connections which are found on the neurosecretory cells⁶, or through substances reaching the neurohypophysis from adjacent tissues. The observation of enkephalin-containing fibres⁷ and opiate receptors²³ within the neurohypophysis, and the presence of large amounts of β-endorphin in the adjacent parts of the pituitary gland^8–10, make these endogenous opioids possible candidates for such a function. Studies of lactation in mice suggest that opiates block the release of oxytocin¹¹, while a considerable body of evidence suggests that the reverse is true regarding the release of vasopressin^12,13. We provide here evidence that opiates inhibit the electrically induced release of oxytocin by an action on or close to the axon terminals within the neurohypophysis, and combine this with evidence to suggest that endogenous opioids tonically suppress the release of oxytocin in response to physiological stimuli.