The abnormal secretion of prolactin (PRL), adrenocorticotropin (ACTH) and/or beta-endorphin (beta-END) has been shown to dramatically affect reproductive function. Elucidating the cellular and subcellular nerochemical mechanisms governing the secretion of these hormones should provide insight into possible therapeutic regimens to alleviate reproductive dysfunctions associated with the aberrant secretion of those hormones. We have utilized HPLC with electro-chemical detection for the concurrent evaluation of neurotransmission in four major monoamine neurotransmitter systems, combined with sensitive RIAs for the quantitation of neuropeptides to evaluate changes in these neuronal systems associated with experimental paradigms where dynamic changes in the secretion of PRL, ACTH and beta- END are occurring. Specific pharmacological antagonists and specialized surgical procedures have been used in vivo as well as in vitro to evaluate the physiological significance, site(s) of action and interaction, and functional neuronal connectivity of individual neurotransmitters in governing the release of these hormones. Our recent results have demonstrated (1) a differential control of PRL secretion were oxytocin plays a major role in the preovulatory surge of PRL in the normal cycling female rat but not in the increases associated with 5-hydroxytryptophan injection, acute suckling or ether vapor stress, (2) strong evidence for a tonic stimulatory role of central epinephrine neurons in regulating corticotropin releasing factor levels in the hypothalamus as well as a vital role in the ether vapor stress- induced increase in plasma ACTH, and (3) an important role for the neurointermediate pituitary (NIL) in (a) the presentation of stress-related increases of these hormones, (b) maintaining hypothalamic levels of some neuropeptide transmitters, and (c) regulating the responsiveness of the anterior pituitary to some known physiological releasing factors. Future experiments will attempt to clarify further the neurochemical mechanisms and the role of the NIL in the physiological regulation of PRL, ACTH and beta-END secretion.
