Brain opiates and neuroendocrine function

Abstract

Opioid peptides are found throughout the central nervous system, and have profound effects on neuroendocrine function. In man, exogenous opiates and opioids elevate circulating prolactin, GH and TSH, and suppress the release of the gonadotrophins and pro-opiocortin-related peptides. However, unlike in other species, there is substantial evidence for a physiological role of endogenous opioids only in the case of the gonadotrophins and ACTH/LPH. Most evidence suggests that LH and FSH are modulated via the hypothalamus or amygdala, where concentrations of opioids and opioid receptors are very high. Endogenous opioids appear to be principally concerned with the frequency-modulated release of GnRH, and this may be important clinically in patients presenting with amenorrhoea. ACTH/LPH are under tonic inhibition by endogenous opioids acting at hypothalamic and/or pituitary levels, and changes in this inhibition may be responsible for the release of these peptides in response to certain forms of stress. It has been reported that the opiate antagonist, naloxone, is clinically useful in paradoxically inhibiting the release of ACTH in patients with Nelson's syndrome, but this requires adequate confirmation. Vasopressin is under biphasic opiate control, but the principal effect is probably opiate-mediated inhibition of vasopressin release. The endogenous ligand for this response is likely to be dynorphin. Suppression of vasopressin release by opiates may become a useful therapy in the treatment of the 'Syndrome of inappropriate ADH'.