Late Pregnancy is a Critical Period for Changes in Phosphorylated Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase 1/2 in Oxytocin Neurones

The physiological demands of parturition and lactation lead to the increased pulsatile release of oxytocin (OT) into the circulation from the neurohypophysial axons of OT neurones in the supraoptic (SON) and paraventricular (PVN) nuclei. These states of increased OT release are accompanied by a sign...

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Veröffentlicht in:Journal of neuroendocrinology 2016-09, Vol.28 (9), p.np-n/a
Hauptverfasser: Chandaka, G. K., Wang, L., Senogles, S., Armstrong, W. E.
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Sprache:eng
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Zusammenfassung:The physiological demands of parturition and lactation lead to the increased pulsatile release of oxytocin (OT) into the circulation from the neurohypophysial axons of OT neurones in the supraoptic (SON) and paraventricular (PVN) nuclei. These states of increased OT release are accompanied by a significant plasticity in magnocellular OT neurones and their synaptic connections, and many of these changes require activation of a central OT receptor. The mitogen‐activated protein kinase/extracellular signal‐regulated kinase pathway (MAPK/ERK) is assumed to be up‐regulated in the PVN during lactation, and many of the effects of OT in peripheral and brain tissue are mediated through a MAPK/ERK pathway. The present study investigated whether this pathway is altered in the SON and PVN during late pregnancy [embryonic day (E)20–21], which is a critical period for OT plasticity induction, and for lactation, when plastic changes are sustained. Based on immunoreactivity for phosphorylated ERK1/2 (pERK1/2), the results suggest an enhanced activation of MAPK/ERK pathway in OT neurones specifically during late pregnancy in both the SON and PVN. Although immunoblots from the SON confirm this pregnancy‐associated up‐regulation in late pregnancy, they also suggest enhancement into lactation as well. Together, the results suggest an important role for the MAPK/ERK pathway during reproductive changes in the SON and PVN.
ISSN:0953-8194
1365-2826
DOI:10.1111/jne.12398