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1 Cell Biology and Neuroscience, University of California, Riverside, Riverside, California, United States
* To whom correspondence should be addressed. E-mail: yufengw{at}ucr.edu.
In non-neuronal tissues, activation of oxytocin receptors (OTRs), like other G
q/11 type G-protein coupled receptors (Gq/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 post- synaptic neurons. Indomethacin also blocked the excitatory effects of phenylephrine, another Gq/11/GPCR activating agent, but not those of PGE2, a non-Gq/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 Gq/11/GPCR-activating agents in neuronal function.
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