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Mechanisms Underlying Oxytocin-Induced Excitation of Supraoptic Neurons: Prostaglandin Mediation of Actin Polymerization

Department of Cell Biology and Neuroscience, University of California, Riverside, California

Submitted 2 December 2005; accepted in final form 10 March 2006

In nonneuronal tissues, activation of oxytocin receptors (OTRs), like other G_q/11 type G-protein-coupled receptors (G_q/11/GPCRs), increase prostaglandin (PG) expression. This is not known for the OTRs expressed by central OT neurons. We examined mechanisms underlying OT's effects on supraoptic nucleus (SON) OT and vasopressin (VP) neurons in hypothalamic slices from lactating rats. OT application (10 pM, 10 min) significantly increased firing rates of OT and VP neurons, both of which expressed OTRs. Indomethacin, an inhibitor of PG synthetases, blocked these increases. OTR (but not a V₁ receptor) antagonist blocked OT effects without blocking the excitatory effect of PGE₂. Tetanus toxin blocked OT effects on fast synaptic inputs and firing activity of SON neurons but not OT-evoked depolarization, suggesting involvement of both pre- and postsynaptic neurons. Indomethacin also blocked the excitatory effects of phenylephrine, another G_q/11/GPCR activating agent but not those of PGE₂, a non-G_q/11/GPCR activating agent in the SON. OT or phenylephrine, but not glutamate or KCl, enhanced cyclooxygenase 2 expression at cytosolic loci in SON neurons and nearby astrocytes, as revealed by immunocytochemistry. This OT effect was not blocked by TTX. Western blot analyses showed that OT significantly increased cyclooxygenase 2 but not actin expression. OT promoted the formation of filamentous actin (F-actin) networks at membrane subcortical areas of both OT and VP neurons. Indomethacin blocked enhancement of F-actin networks by OT but not by PGE₂. These results indicate that PGs serve as a common mediator of G_q/11/GPCR-activating agents in neuronal function.

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