Opioid peptide- as well as vasopressin-containing neurons synapse on gonadotropin releasing hormone neurons in juvenile macaques. In this study we performed double-label immunostaining for opioid and vasopressin neurons in the paraventricular and supraoptic nuclei in order to assess their interrelationships. Neuroendocrine neurons in the hypothalamus were prelabeled by microinjection of electron-dense retrograde tracer into the median eminence, and were easily identified in frontal Vibratome sections. Sections through the paraventricular and supraoptic nuclei were immunostained for vasopressin with the peroxidase-antiperoxidase technique, and for opioids using the indirect immunogold method. By light microscopy, opioid-immunoreactive inputs appeared to innervate an average of 39% of the vasopressin neurons in the paraventricular nucleus and 33% in the supraoptic nucleus, and were more prevalent anteriorly. Clusters of opioid afferents formed cup-like calices around major processes of many vasopressin neurons, especially in the paraventricular nucleus. Electron microscopy revealed that these groups of opioid axon terminals made frequent symmetrical and fewer asymmetrical synapses on both neuroendocrine and non-neuroendocrine vasopressinergic cell bodies and dendrites. Our study did not reveal vasopressin opioid synapses in these hypothalamic nuclei, but this does not preclude the possibility of their existence elsewhere. These results indicate that opioid afferents modulate vasopressin neuronal activity in the monkey paraventricular and supraoptic nuclei. Previous results have suggested that corticotropin releasing hormone acts via vasopressinergic neurons to stimulate opioid neuronal activity and to inhibit gonadotropin releasing hormone release. Taken together, the data suggest that stressful stimuli could initiate a series of neuropeptidergic interactions which ultimately alter pulsatile gonadotropin releasing hormone secretion and thus gonadotropin secretion in primates.
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