Intracellular calcium stores regulate activity-dependent neuropeptide release from dendrites

Mike Ludwig (), Nancy Sabatier, Philip M. Bull, Rainer Landgraf, Govindan Dayanithi and Gareth Leng
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Mike Ludwig: University of Edinburgh Medical School
Nancy Sabatier: University of Edinburgh Medical School
Philip M. Bull: University of Edinburgh Medical School
Rainer Landgraf: Max Planck Institute of Psychiatry, Clinical Institute
Govindan Dayanithi: University of Montpellier II
Gareth Leng: University of Edinburgh Medical School

Nature, 2002, vol. 418, issue 6893, 85-89

Abstract: 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 terminals1,2,3,4. 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.

Date: 2002
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DOI: 10.1038/nature00822

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