Oxytocin-induced postinhibitory rebound firing facilitates bursting activity in oxytocin neurons.

J.-M. Israel, D. A. Poulain, S. H. R. Oliet
Journal of Neuroscience. 2008-01-09; 28(2): 385-394
DOI: 10.1523/JNEUROSCI.5198-07.2008

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During parturition and lactation, neurosecretory oxytocin (OT) neurons in the
hypothalamus achieve pulsatile hormone secretion by coordinated bursts of firing
that occur throughout the neuronal population. This activity is partly controlled
by somatodendritic release of OT, which facilitates the onset and recurrence of
synchronized bursting. To further investigate the cellular mechanisms underlying
the control exerted by OT on the activity of its own neurons, we studied the
effects of the peptide on membrane potential and synaptic activity in OT neurons
in hypothalamic organotypic slice cultures. Bath application of low
concentrations of OT (100 nM. As shown previously, higher concentrations of OT (>500
nM) had the opposite effect, inhibiting GABA(A) receptors via a postsynaptic
mechanism. Surprisingly, OT-mediated facilitation of GABAergic transmission
promoted action potential firing in 40% of the neurons. Each action potential
occurred at the end of the repolarizing phase of an inhibitory potential.
Pharmacological dissection revealed that this firing involved the activation of
low-threshold activated calcium channels. Detailed statistical analysis showed
that OT-mediated firing upregulated bursting activity in OT neurons. It is thus
likely to optimize OT secretion and, as a consequence, facilitate delivery and
milk ejection in mammals.


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