Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville, United States
Yalun Tan
Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville, United States; Department of Anesthesiology, School of Medicine, Stanford University, Stanford, United States
Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville, United States; Center for Integrative Cardiovascular and Metabolic Diseases, University of Florida, Gainesville, United States; Evelyn F. and William L. McKnight Brain Institute, University of Florida, Gainesville, United States
Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville, United States; Center for Integrative Cardiovascular and Metabolic Diseases, University of Florida, Gainesville, United States
Hypothalamic oxytocinergic magnocellular neurons have a fascinating ability to release peptide from both their axon terminals and from their dendrites. Existing data indicates that the relationship between somatic activity and dendritic release is not constant, but the mechanisms through which this relationship can be modulated are not completely understood. Here, we use a combination of electrical and optical recording techniques to quantify activity-induced 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; however, activity-induced dendritic calcium influx can be robustly regulated by both osmosensitive and non-osmosensitive ion channels located along the dendritic membrane. Overall, this study reveals that dendritic conductivity is a dynamic and endogenously regulated feature of OT-MCNs that is likely to have substantial functional impact on central oxytocin release.
