Dendritic membrane resistance modulates activity-induced Ca2+ influx in oxytocinergic magnocellular neurons of mouse PVN

Hypothalamic oxytocinergic magnocellular neurons have a fascinating ability to release peptide from both their axon terminals and from their dendrites. Existing data indicates there is a flexible relationship between somatic activity and dendritic release, but the mechanisms governing this relationship are not completely understood. Here we use a combination of electrical and optical recording techniques to quantify activity-dependent calcium influx in proximal vs. distal dendrites of oxytocinergic magnocellular neurons located in the paraventricular nucleus of the hypothalamus (OT-MCNs). Results reveal that the dendrites of OT-MCNs are weak conductors of somatic voltage changes, and yet activity-induced dendritic calcium influx can be robustly regulated by a diverse set of stimuli that open or close ionophores located along the dendritic membrane. Overall, this study reveals that dendritic membrane resistance is a dynamic and endogenously regulated feature of OT-MCNs that is likely to have substantial functional impact on central oxytocin release. IMPACT STATEMENTActivity-induced dendritic calcium influx in oxytocinergic magnocellular neurons can be robustly modulated by a highly diverse set of stimuli acting on distinct types of ionophores expressed along the dendritic membrane.