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Intracellular calcium stores regulate activity-dependent neuropeptide release from dendrites

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.

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Figure 1: Oxytocin release in the SON.
Figure 2: Effects of intracellular calcium mobilizers (horizontal bars) on oxytocin release in vitro.
Figure 3: The effects of CCS (a) on a representative oxytocin cell (be), and data from 11 cells exposed to CCS after thapsigargin (f, g).
Figure 4: The effects of CCS on a representative oxytocin cell.

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Acknowledgements

The work was supported by the European Union, the Wellcome Trust, the DAAD/ARC, the British Council and the Alliance Franco-British Partnership Programme.

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Correspondence to Mike Ludwig.

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Ludwig, M., Sabatier, N., Bull, P. et al. Intracellular calcium stores regulate activity-dependent neuropeptide release from dendrites. Nature 418, 85–89 (2002). https://doi.org/10.1038/nature00822

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