Ionic and signaling mechanisms involved in neurotensin-mediated excitation of central amygdala neurons.
Ionic and signaling mechanisms involved in neurotensin-mediated excitation of central amygdala neurons.
复制标题
中央杏仁核神经元的神经素介导的激发涉及的离子和信号传导机制。
DOI：
10.1016/j.neuropharm.2021.108714
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发表时间：
2021-09-15
影响因子：
4.7
通讯作者：
Hu B
中科院分区：
文献类型：
--
作者：
Lei S;Hu B
神经降压素(NT)在大脑中起着神经调节剂的作用，调节着多种生理功能。虽然中央杏仁核(CEA)表达NT肽和NTS1受体，NT的应用已被证明能兴奋CEA神经元，但其潜在的细胞和分子机制尚未确定。我们发现NTS1受体的激活增加了CEA外侧核(CEL)的神经元兴奋性。NT引起的神经细胞兴奋需要磷脂酶Cβ(PLCβ)和磷脂酰肌醇4，5-二磷酸(PIP2)的耗竭，而细胞内钙离子的释放和PKC不是必需的。NT可增加CEL神经元的输入电阻和时间常数，提示NT通过降低细胞膜电导来兴奋CEL神经元。NT引起的细胞兴奋需要抑制包括Kir2亚家族和GIRK通道在内的内向整流钾(KIR)通道。细胞中NTS1受体的激活导致CEA神经元内侧核的GABA能抑制，提示NT调节杏仁核的网络活动。我们的结果可能为解释NT在体内的生理功能提供了细胞和分子机制。
Neurotensin (NT) serves as a neuromodulator in the brain where it regulates a variety of physiological functions. Whereas the central amygdala (CeA) expresses NT peptide and NTS1 receptors and application of NT has been shown to excite CeA neurons, the underlying cellular and molecular mechanisms have not been determined. We found that activation of NTS1 receptors increased the neuronal excitability of the lateral nucleus (CeL) of CeA. Both phospholipase Cβ (PLCβ) and phosphatidylinositol 4,5-bisphosphate (PIP2) depletion were required, whereas intracellular Ca2+ release and PKC were unnecessary for NT-elicited excitation of CeL neurons. NT increased the input resistance and time constants of CeL neurons, suggesting that NT excites CeL neurons by decreasing a membrane conductance. Depressions of the inwardly rectifying K+ (Kir) channels including both the Kir2 subfamily and the GIRK channels were required for NT-elicited excitation of CeL neurons. Activation of NTS1 receptors in the CeL led to GABAergic inhibition of medial nucleus of CeA neurons, suggesting that NT modulates the network activity in the amygdala. Our results may provide a cellular and molecular mechanism to explain the physiological functions of NT in vivo.
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