This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator.
The aim of this proposal is to understand the mechanisms by which daylight drives a specific sensory-neuroendocrine system to regulate changes in prolactin secretion. Clear evidence from research on sheep shows that daylight regulates melatonin output from the pineal gland, which in turn, controls prolactin secretion from the pars distalis of the the pituitary gland. This effect is transduced through a specific factor released by the pars tuberalis of the pituitray gland. The identity of this pars tuberalis factor and how it regulates prolactin release is unknown. Based on strong preliminary data, we hypothesize that this factor is a tachykinin. The proposed research will utilize a combination of studies to determine the in vivo secretion of tachykinins into the hypophyseal portal circulation and the effects of tachykinins on prolactin release. Immunocytochemical and RT-PCR studies will establish how daylight, through melatonin, drives changes in the cellular secretory machinery of the pars tuberalis. This research will challenge the prevailing dogma that prolactin regulation is solely driven through factors of neuronal origin. It will provide novel insight into a fundamental sensory-neuroendocrine system and elucidate the specific mechanisms whereby daylight drives this system. It will also generate new insight into potential causes of idiosyncratic hyperprolactinemia, especially those generated by the so-called """"""""stalk-effect"""""""".
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