Performance, properties and plasticity of identified oxytocin and vasopressin neurones in vitro.
Performance, properties and plasticity of identified oxytocin and vasopressin neurones in vitro.
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DOI：
10.1111/j.1365-2826.2010.01989.x
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发表时间：
2010-05
影响因子：
3.2
通讯作者：
Teruyama R
中科院分区：
文献类型：
--
作者：
Armstrong WE;Wang L;Li C;Teruyama R
神经垂体激素催产素 (OT) 和加压素 (VP) 源自室旁核和视上核 (SON) 的下丘脑神经分泌细胞。这些神经元产生的动作电位的放电率和模式决定了外周激素释放的时间和数量。我们在体外对下丘脑切片中充满生物胞素的 SON 神经元进行免疫化学鉴定，以揭示 OT 和 VP 神经元在膜和突触特性、放电模式以及怀孕和哺乳期间可塑性方面的差异。在这篇综述中，我们总结了这种方法的一些最新发现：1）VP 神经元兴奋性受到相爆发活动背后的慢（sDAP）和快（fDAP）去极化后电位的影响。 fDAP 可能与瞬态受体电位 (TRP) 通道、褪黑素型（TRPM4 和/或 TRPM5）有关，这两种通道在免疫化学上更多地定位于 VP 神经元，尤其是其树突。 TRPM4 和 TRPM5 mRNA 均在 SON 中发现，但单细胞 RT-PCR 表明 TRPM4 可能是更重要的通道。 VP 神经元的相位爆发几乎不受切片中自发突触活动的影响，主要由内在电流形成。 2) OT 神经元的放电模式范围从不规则到连续，变异系数由随机分布的自发 GABA 能抑制性突触电流 (sIPSC) 决定。这些 sIPSC 在 OT 神经元中的出现频率是 VP 神经元的 4-5 倍，并且比自发兴奋性突触电流要频繁得多。 3) 两种细胞类型均表达 Ca++ 依赖性后超极化 (AHP)，包括 apamin 敏感、中等持续时间的 AHP 和较慢、apamin 不敏感的 AHP (sAHP)。在 OT 神经元中，两种 AHP 在怀孕和哺乳期间都会增强。在怀孕期间，sAHP 的可塑性被中枢 OT 受体的拮抗作用所阻断。通过将第 19 天怀孕大鼠的切片暴露于 OT 和雌二醇来模拟 AHP 增强，这表明中枢 OT 和性类固醇在怀孕期间通过直接下丘脑作用来编程这种可塑性。总之，VP 和 OT 神经元功能的差异是由膜和突触特性的差异造成的，并受到生殖状态的差异调节。
The neurohypophysial hormones oxytocin (OT) and vasopressin (VP) originate from hypothalamic neurosecretory cells in the paraventricular and supraoptic (SON) nuclei. The firing rate and pattern of action potentials arising from these neurones determine the timing and quantity of peripheral hormone release. We have used immunochemical identification of biocytin-filled SON neurones in hypothalamic slices in vitro to uncover differences between OT and VP neurones in membrane and synaptic properties, firing patterns, and plasticity during pregnancy and lactation. In this review we summarise some recent findings from this approach: 1) VP neuronal excitability is influenced by slow (sDAP) and fast (fDAP) depolarising afterpotentials that underlie phasic bursting activity. The fDAP may relate to a transient receptor potential (TRP) channel, type melastatin (TRPM4 and/or TRPM5), both of which are immunochemically localised more to VP neurones, and especially, to their dendrites. Both TRPM4 and TRPM5 mRNAs are found in the SON, but single cell RT-PCR suggestsTRPM4 might be the more prominent channel. Phasic bursting in VP neurones is little influenced by spontaneous synaptic activity in slices, being shaped largely by intrinsic currents. 2) The firing pattern of OT neurones ranges from irregular to continuous, with the coefficient of variation determined by randomly distributed, spontaneous GABAergic, inhibitory synaptic currents (sIPSCs). These sIPSCs are 4–5 fold more frequent in OT vs. VP neurones, and much more frequent than spontaneous excitatory synaptic currents. 3) Both cell types express Ca++-dependent afterhyperpolarisations (AHPs), including an apamin-sensitive, medium duration AHP and a slower, apamin-insensitive AHP (sAHP). In OT neurones, both AHPs are enhanced during pregnancy and lactation. During pregnancy, the plasticity of the sAHP is blocked by antagonism of central OT receptors. AHP enhancement is mimicked by exposing slices from Day 19 pregnant rats to OT and oestradiol, suggesting central OT and sex steroids program this plasticity during pregnancy by direct hypothalamic actions. In conclusion, the differences in VP and OT neuronal function are underlain by differences in both membrane and synaptic properties, and differentially modulated by reproductive state.
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