Please cite this article in press as: Schröder, I., et al., Laboratory safety attitudes and practices: A comparison of academic, government, and industry researchers, J. Chem. Health Safety (2015), http://dx.

Seasonal reproduction in the ewe is generated by an endogenous circannual rhythm of reproductive neuroendocrine activity. Exposure to as few as 70 days of photoperiodic information a year is sufficient to synchronize the rhythm. The present study was conducted to identify which portions of the photoperiodic cycle are utilized for synchronization. For this purpose, we used pinealectomized ewes that could not respond reproductively to changes in day length. Selected photoperiodic information was provided via infusion of melatonin, a hormone that provides the neuroendocrine code for day length in this species. Melatonin was delivered according to circadian patterns. The infusion patterns were tailored to mimic those of melatonin secretion in pineal-intact ewes during one of the four seasons: winter, spring, summer, or autumn. The infusions were provided for 90 days a year during each of the three years following pinealectomy. The ewes were ovariectomized and treated with constant-release Silastic capsules containing estradiol; reproductive neuroendocrine activity was monitored by measurement of serum concentrations of LH. In the absence of exogenous melatonin, most (19 of 24) pinealectomized controls exhibited circannual LH cycles that were not in synchrony, indicating that the rhythm was free-running. Melatonin synchronized the rhythm (such that the period was 365 days and the stages of the rhythm were both concurrent among animals and in appropriate phase with the geophysical year), but not all melatonin patterns were equally effective in this regard. The most effective melatonin patterns mimicked those of secretion during summer. Spring and autumn melatonin patterns were less effective, and winter melatonin patterns were ineffective. These results support the concept that there is a seasonal specificity with regard to the photoperiodic cues that synchronize the circannual rhythm of reproductive neuroendocrine activity in the ewe. The rhythm is synchronized most effectively by long-day photoperiodic cues perceived on or around the summer solstice.

Bisphenol A (BPA) is a well-known environmental, endocrine-disrupting chemical, and bisphenol S (BPS) has been considered a safer alternative for BPA-free products. The present study aims to evaluate the impact of BPA and BPS on the reproductive neuroendocrine system during zebrafish embryonic and larval development and to explore potential mechanisms of action associated with estrogen receptor (ER), thyroid hormone receptor (THR), and enzyme aromatase (AROM) pathways. Environmentally relevant, low levels of BPA exposure during development led to advanced hatching time, increased numbers of GnRH3 neurons in both terminal nerve and hypothalamus, increased expression of reproduction-related genes (kiss1, kiss1r, gnrh3, lhβ, fshβ, and erα), and a marker for synaptic transmission (sv2). Low levels of BPS exposure led to similar effects: increased numbers of hypothalamic GnRH3 neurons and increased expression of kiss1, gnrh3, and erα. Antagonists of ER, THRs, and AROM blocked many of the effects of BPA and BPS on reproduction-related gene expression, providing evidence that those three pathways mediate the actions of BPA and BPS on the reproductive neuroendocrine system. This study demonstrates that alternatives to BPA used in the manufacture of BPA-free products are not necessarily safer. Furthermore, this is the first study to describe the impact of low-level BPA and BPS exposure on the Kiss/Kiss receptor system during development. It is also the first report of multiple cellular pathways (ERα, THRs, and AROM) mediating the effects of BPA and BPS during embryonic development in any species.

The insulin receptor is a tyrosine kinase receptor that is found in mammalian brain and at high concentrations in the bag cell neurons of Aplysia. We show here that insulin causes an acute rise in intracellular Ca2+ concentration ([Ca2+]i) in these neurons and triggers release of neuropeptide. The insulin-sensitive intracellular Ca2+ pool differs pharmacologically from previously described Ca2+ stores that are sensitive to inositol trisphosphate and from mitochondrial Ca2+ stores. Insulin, but not thapsigargin, stimulates Ca2+ release at the distal tips of neurites, the presumed site of neuropeptide secretion. The effects of insulin on intracellular Ca2+ release and neuropeptide secretion occur without triggering spontaneous action potentials. The insulin-sensitive rise in [Ca2+]i moves into the distal tips of neurites after exposure to a cyclic AMP analogue, a treatment that causes a similar translocation of neuronal vesicles. Our data indicate that Ca2+ release from a distinct intracellular pool associated with secretory vesicles may contribute to secretion of neuropeptide in the absence of neuronal discharge.

No abstract