Central neurokinin 3 receptors increase systemic oxytocin release: interaction with norepinephrine.

Central neurokinin 3 receptors increase systemic oxytocin release: interaction with norepinephrine.
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中枢神经激肽 3 受体增加全身催产素释放:与去甲肾上腺素相互作用。

DOI:
10.1016/j.expneurol.2003.08.012
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发表时间:
2003
期刊:
Experimental neurology.
影响因子:
--
通讯作者:
Flynn,FrancisW
Flynn,FrancisW
中科院分区:
--
文献类型:
--
作者:
Bealer,StevenL;Flynn,FrancisW

文献摘要

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Stimulation of central tachykinin receptors contributes to neuroendocrine functions of the hypothalamo-neurohypophyseal system. However, the specific role of each tachykinin receptor subtype has not been completely characterized. Specifically, while neurokinin 3 (NK3) receptor stimulation increases systemic vasopressin, the effects on oxytocin (OT) are not known. Therefore, the present studies investigated the effect of central NK3 receptor stimulation with senktide on release of systemic and central OT. Furthermore, since central NK3 receptors activate noradrenergic systems, which contribute to OT release, the effects of α-adrenergic receptor blockade on senktide-induced changes in OT release were evaluated. Female rats were implanted with a cannula in the third cerebral ventricle, and changes in plasma OT concentration determined before and following central administration of senktide in vehicle-treated rats, and animals following central administration of the α-adrenergic antagonist phentolamine. Other rats were implanted with microdialysis probes adjacent to the paraventricular nucleus (PVN), and dialysate and plasma OT concentrations were determined before and during administration of senktide through the dialysis probe. Central senktide increased systemic OT release, which was prevented by pretreatment with phentolamine. Furthermore, there was no detectable change in extracellular OT concentration in the PVN during dialysis administration of senktide. These data demonstrate that activation of central NK3 receptors stimulates systemic release of OT by activation of central noradrenergic systems, apparently without increasing intranuclear OT release in the PVN.