Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.24.169466v1?rss=1 Authors: Francesconi, W., Berton, F., Olivera-Pasilio, V., Dabrowska, J. Abstract: The dorsolateral bed nucleus of the stria terminalis (BNSTDL) has high expression of oxytocin (OT) receptors (OTR), which were shown to facilitate cued fear. The BNSTDL contains GABA-ergic neurons classified based on intrinsic membrane properties into three major types. Using in vitro patch-clamp recordings in male rats, we demonstrate that OT selectively excites Type I neurons in an OTR-dependent manner as revealed by a significantly increased resting membrane potential, increased input resistance, reduced rheobase, reduced fast and medium spike afterhyperpolarization, reduced threshold and latency to a first spike, as well as a left shift in the spike frequency/current relationship. As Type I neurons are putative BNSTDL interneurons, we next recorded inhibitory synaptic transmission in all three types of neurons and we demonstrate that OT increases the frequency, but not amplitude, of spontaneous inhibitory post-synaptic currents (sIPSCs), selectively in Type II neurons. This effect was abolished by the presence of an OTR antagonist or tetrodotoxin, the latter suggesting an indirect effect via an OT-induced increase in firing of Type I interneurons. As Type II neurons were shown to project to the central amygdala (CeA), we also recorded from retrogradely labeled BNST{Rightarrow}CeA neurons, which we identified as Type II. These results present a model of fine-tuned modulation of intrinsic BNSTDL neurocircuitry by OT, which selectively excites Type I neurons, leading to increased GABA-ergic inhibition in Type II projection neurons. Lastly, we demonstrate that fear-conditioning increases sIPSCs frequency in Type II neurons, mimicking the effect of OT. Based on the findings, we propose that OTR in the BNSTDL facilitate cued fear by inhibiting BNST{Rightarrow}CeA neurons. Copy rights belong to original authors. Visit the link for more info