Intracellular calcium stores regulate activity-dependent neuropeptide release from dendrites

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, transmitti...

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Bibliographic Details
Published in:Nature (London) 2002-07, Vol.418 (6893), p.85-89
Main Authors: Ludwig, Mike, Sabatier, Nancy, Bull, Philip M, Landgraf, Rainer, Dayanithi, Govindan, Leng, Gareth
Format: Article
Language:English
Subjects:
Animals
Calcium
Calcium - metabolism
Calcium Signaling - drug effects
Central nervous system
Dendrites
Dendrites - drug effects
Dendrites - metabolism
Dendrites - secretion
Electrophysiology
Female
Microdialysis
Neurology
Neurons
Neuropeptides - secretion
Oxytocin - secretion
Peptides
Rats
Supraoptic Nucleus - cytology
Supraoptic Nucleus - drug effects
Supraoptic Nucleus - metabolism
Supraoptic Nucleus - secretion
Synapses - drug effects
Synapses - metabolism
Synapses - secretion
Thapsigargin - pharmacology
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Summary: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. 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 compartments. Here, we show that in hypothalamic oxytocin neurons, agents that mobilize intracellular Ca(2+) 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 Ca(2+) 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.
ISSN:0028-0836
1476-4687
DOI:10.1038/nature00822