Reproductive hazards associated with exposure to nitrous oxide: Epidemiological data from human and animal studies indicate that chronic exposure to nitrous oxide (N2O) results in impaired reproductive function and decreased fertility rates. Preliminary studies performed in our laboratory indicate that N2O exposure disrupts estrous cyclicity with concomitant alterations in diencephalic opioid peptide concentrations, catecholamine turnover rates, and gonadotropin-releasing hormone (GnRH) concentrations. Furthermore, in vitro studies performed in our laboratory, utilizing immortalized GnRH neurons (GT1-7 cells), indicate that exposure to N2O results in significant decreases in proGnRH mRNA concentrations. These results are consistent with our overall hypothesis that N2O impairs hypothalamic control of gonadotropin release, either by directly acting on GnRH neurons or by altering upstream neural influences on GnRH neurons.
Effects of lead exposure during early development on neural circuits controlling puberty onset and hypothalamic-pituitary axis: This is a collaborative research effort with Drs. Dees and Bratton at Texas A&M University. We will examine the effects of LEAD on the molecular and cellular events upstream of the GnRH neuron crucial to gonadotropin secretion regulation, as well as signaling pathways, and metabolism of GnRH peptide in cultured GT1-7 cells.