Experiments by the Reproductive Neuroendocrinology Section focus on the identification and development of cellular and subcellular mechanisms involved in the regulation of pituitary hormone secretion, in particular, prolactin (PRL), adrenocorticotrophin (ACTH), and Beta-endorphin (Beta-end). Specific studies are designed to elucidate the role and interactions of monoaminergic neurotransmitters and peptide releasing and release-inhibiting hormones in the secretory control of these hormones from the anterior (AP) and neurointermediate (NIL) lobes of the pituitary, the sequential arrangement and possible connectivity of that neuronal circuitry, and the developmental maturation of that circuitry. Furthermore, various stressful stimuli not only dramatically affect reproductive function as well as the secretion of PRL, ACTH, and Beta-end, but the stress-induced increase in plasma PRL has also been shown to require a developmental maturation postnatally. Therefore, this paradigm has been utilized to selectively examine the neuronal mechanisms involved in the stress-induced increase in PRL secretion. In addition, drugs which interact selectively with specific neurotransmitter or neuropeptide neuronal systems are utilized to determine the individual contributions of specific neuronal systems to the regulatory secretion of PRL, ACTH, and Beta-end, and to aid in elucidating the neuronal connectivity involved in that regulation. Lastly, specific lesions and surgical procedures are employed to determine the source of various neurotransmitters and neuropeptides which are found in the pituitary or have been shown to act at the pituitary level, and the role that those neurotransmitters/neuropeptides play in the dynamic regulation of PRL, ACTH, and Beta-end secretion. These studies are integrated to elucidate the neuronal mechanisms, integration, and connectivity involved in the neuroendocrine regulation of the secretion of particular hormones from the pituitary which have been shown capable of affecting reproductive function.