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Abstract：
Oxytocin and vasopressin secretion from the posterior pituitary gland are required for normal pregnancy and lactation. Oxytocin secretion is relatively low and constant under basal conditions but becomes pulsatile during birth and lactation to stimulate episodic contraction of the uterus for delivery of the fetus and milk ejection during suckling. Vasopressin secretion is maintained in pregnancy and lactation despite reduced osmolality (the principal stimulus for vasopressin secretion) to increase water retention to cope with the cardiovascular demands of pregnancy and lactation. Oxytocin and vasopressin secretion are determined by the action potential (spike) firing of magnocellular neurosecretory neurons of the hypothalamic supraoptic and paraventricular nuclei. In addition to synaptic input activity, spike firing depends on intrinsic excitability conferred by the suite of channels expressed by the neurons. Therefore, we analysed oxytocin and vasopressin neuron activity in anaesthetised non-pregnant, late-pregnant, and lactating rats to test the hypothesis that intrinsic excitability of oxytocin and vasopressin neurons is increased in late pregnancy and lactation to promote oxytocin and vasopressin secretion required for successful pregnancy and lactation. Hazard analysis of spike firing revealed a higher incidence of post-spike hyperexcitability immediately following each spike in oxytocin neurons, but not in vasopressin neurons, in late pregnancy and lactation, which is expected to facilitate high frequency firing during bursts. Despite lower osmolality in late-pregnant and lactating rats, vasopressin neuron activity was not different between non-pregnant, late-pregnant, and lactating rats, and blockade of osmosensitive ΔN-TRPV1 channels inhibited vasopressin neurons to a similar extent in non-pregnant, late-pregnant, and lactating rats. Furthermore, supraoptic nucleus ΔN-TRPV1 mRNA expression was not different between non-pregnant and late-pregnant rats, suggesting that sustained activity of ΔN-TRPV1 channels might maintain vasopressin neuron activity to increase water retention during pregnancy and lactation.
摘要：
正常妊娠和哺乳需要垂体后叶分泌催产素和加压素。催产素分泌在基础条件下相对较低且恒定，但在出生和哺乳期间变得脉动，以刺激子宫的间歇性收缩，以分娩胎儿并在哺乳期间排出乳汁。尽管降低了渗透压（血管加压素分泌的主要刺激）以增加水潴留以应对怀孕和哺乳的心血管需求，但血管加压素分泌在怀孕和哺乳期间仍得以维持。催产素和加压素的分泌取决于下丘脑视上和室旁核的大细胞神经分泌神经元的动作电位（尖峰）放电。除了突触输入活动，尖峰放电取决于神经元表达的一套通道赋予的内在兴奋性。因此,我们分析了催产素和加压素在麻醉的非孕妇的神经元活性，晚孕,和哺乳期大鼠来检验以下假设：在妊娠晚期和哺乳期，催产素和加压素神经元的内在兴奋性增加，以促进成功妊娠和哺乳期所需的催产素和加压素分泌。尖峰放电的危害分析显示，在催产素神经元的每个尖峰之后，尖峰后过度兴奋的发生率更高，但不是在加压素神经元中，在怀孕后期和哺乳期，这有望促进突发期间的高频发射。尽管妊娠晚期和哺乳期大鼠的渗透压较低，血管加压素神经元活性在非孕妇之间没有差异，晚孕,和哺乳期的老鼠，和渗透敏感性ΔN-TRPV1通道的阻断抑制血管加压素神经元在非妊娠的相似程度，晚孕,和哺乳大鼠。此外，视上核ΔN-TRPV1mRNA表达在非妊娠和晚期妊娠大鼠之间没有差异，提示ΔN-TRPV1通道的持续活性可能会维持加压素神经元的活性，从而增加妊娠和哺乳期的水潴留。
