1. Department of Biomedical Sciences, University of Edinburgh Medical School, George Square, Edinburgh EH8 9XD, UK
2. Max Planck Institute of Psychiatry, Clinical Institute, Kraepelinstrae 2-10, 80804 Munich, Germany
3. Department of Neurobiology, INSERM 432, University of Montpellier II, Place Eugene Bataillon, F-34094 Montpellier, Cedex 5, France

Correspondence to: Mike Ludwig¹ Correspondence and requests for materials should be addressed to M.L. (e-mail: Email: mike.ludwig@ed.ac.uk).

Abstract

Information in neurons flows from synapses, through the dendrites and cell body (soma), and, finally, along the axon as spikes of electrical activity that will ultimately release neurotransmitters from the nerve terminals. However, the dendrites of many neurons also have a secretory role, transmitting information back to afferent nerve terminals^{1, 2, 3, 4}. In some central nervous system neurons, spikes that originate at the soma can travel along dendrites as well as axons, and may thus elicit secretion from both compartments¹. Here, we show that in hypothalamic oxytocin neurons, agents that mobilize intracellular Ca²⁺ induce oxytocin release from dendrites without increasing the electrical activity of the cell body, and without inducing secretion from the nerve terminals. Conversely, electrical activity in the cell bodies can cause the secretion of oxytocin from nerve terminals with little or no release from the dendrites. Finally, mobilization of intracellular Ca²⁺ can also prime the releasable pool of oxytocin in the dendrites. This priming action makes dendritic oxytocin available for release in response to subsequent spike activity. Priming persists for a prolonged period, changing the nature of interactions between oxytocin neurons and their neighbours.