摘要

Activation of estrogen receptor beta (ER beta)-expressing neurons regulates the mammalian stress response via the hypothalamic-pituitary-adrenal (HPA) axis. These neurons densely populate the paraventricular nucleus of the hypothalamus (PVN). Recent research has revealed striking differences between rat and mouse PVN cytochemistry, but careful exploration of PVN ER beta neurons in mice has been hindered by a lack of specific ER beta antisera. Therefore, we used male and female transgenic mice expressing EGFP under the control of the mouse ER beta promoter (ER beta-EGFP) to examine the chemical architecture of PVN ER beta cells. Using immunohistochemistry, we found that 90% of ER beta-immunoreactivity (-ir) colocalized with EGFP. Cellular colocalization of EGFP with neuropeptides, transcription modulators, and neuronal tracers was examined throughout the PVN. ERb-EGFP cells expressed oxytocin more abundantly in the rostral (71 +/- 3%) than caudal (33 +/- 8%) PVN. Arginine vasopressin colocalized with EGFP more often in females (18 +/- 3%) than males (4 +/- 1%). Moreover, estrogen receptor a-ir colocalized with ER beta-EGFP at low levels (15 +/- 3%). Using a corticotropin releasing hormone-cre driver X tdTomato reporter mouse, we found a moderate colocalization with ER beta-ir (48 +/- 16%) in the middle PVN. Peripheral injection of fluorogold revealed that the rostral PVN ER beta-EGFP cells are neuroendocrine neurons whereas non-neuroendocrine (presumably pre-autonomic) ER beta-EGFP neurons predominated in the posterior PVN. These data demonstrate chemoarchitectural differences in ER beta neurons of the mouse PVN that are different from that previously described for the rat, thus, elucidating potential neuronal pathways involved in the regulation of the HPA axis in mice.

  • 出版日期2017-12-1