The oxytocinergic neurons of the anterior commissural nucleus: Estrogen effects and mechanisms
Description
The Anterior Commissural Nucleus (ACN) is an hypothalamic accessory nucleus that has been implicated in the expression of maternal behavior. Estrogen increases oxytocin (OT) mRNA levels in the ACN. However, these ACN OT neurons have not been shown to possess estrogen receptors (ER), nor to concentrate $\sp3$H-estradiol. Since these OT neurons are in close proximity to a group of ER-containing cells has led to speculation that an indirect pathway exists for estrogen activation of the ACN OT neurons. In the present study, several of the effects of estrogen on the OT neurons of the ACN were examined, and potential neuronal links between ER-containing cells and OT neurons were explored Using double-labeling immunocytochemistry (ICC), we confirmed that ER was not present in the OT neurons of the ACN. Four daily injections of EB, in comparison to a similar injection schedule with oil, increased by 26% the number of OT-ir neurons (p $<$ 0.001) and by 40% their staining intensity (p $<$ 0.03). A comparison of the distribution of ACN OT-ir neurons in EB- and oil-injected animals suggested a greater increase in cell number in the more rostral areas of the ACN. Eleven neuroactive substances were examined using ICC and in situ hybridization methods to identify the type of neuron in the ACN that might co-localize ER. Dopamine-beta-hydroxylase, neuropeptide Y, tyrosine hydroxylase (TH) and glutamic acid decarboxylase (GAD) were found in the ACN. Only TH and GAD were found in cell bodies. In situ hybridization for GAD mRNA suggested that GAD is present in many of the ER-containing neurons in the ACN. ICC studies confirm that the OT neurons of the ACN co-localize GABA receptor on their membranes. Pseudo-confocal microscopy showed that estrogen treatment resulted in a decrease of glial coverage from 80% of OT neurons examined to 20% (p $<$ 0.05). It was concluded that the glia and OT neurons of the ACN are responsive to estrogen, and that the response of the OT neurons is mediated at least in part by the ER-containing, GABAergic neurons of the ACN