Corticotrophin-releasing factor inhibits neuromedin U mRNA expressing neuron in the rat hypothalamic paraventricular nucleus in vitro
Corticotrophin-releasing factor inhibits neuromedin U mRNA expressing neuron in the rat hypothalamic paraventricular nucleus in vitro
复制标题
促肾上腺皮质激素释放因子体外抑制大鼠下丘脑室旁核表达神经调节素U mRNA的神经元
DOI：
10.1016/j.neulet.2012.01.035
复制
发表时间：
2012-03-09
影响因子：
2.5
通讯作者：
Qiu, De-Lai
中科院分区：
文献类型：
--
作者：
Chu, Chun-Ping;Xu, Chuan-Jie;Qiu, De-Lai
在本研究中，我们检查了整个细胞旁培养基核（PVN）中表达神经蛋白释放因子（CRF）对神经蛋白U（NMU）mRNA表达神经元的影响，该神经元通过全细胞贴片贴片膜片记录和单细胞反转录 - 转录 - 型 - 转录 - 型聚合物聚合物链反应（单电池反应反应）（单细胞反应）技术（单核反应）技术（单电池）技术。总共筛选了NMU mRNA的116个PVN假定的副细胞神经元，其中14.7％（17/116）表达了NMU mRNA。在表达NMU mRNA的神经元中观察到的电生理特性是生成低阈值Ca2+尖峰（LTS）和可靠的低压激活（T型）Ca2+电流。在电流钳条件下，CRF（100 nm）诱导了尖峰射击的可逆下降，并显着降低了NMU mRNA表达神经元的88.2％（15/17）的LTS。选择性CRF受体拮抗剂的1 Mu Mα-螺旋螺旋外施用（9-14）（9-14）（alpha-hcrf）完全阻止了表达NMU mRNA mRNA的神经元中CRF诱导的峰值触发。在电压钳条件下，CRF（100 nm）将T型Ca2 +电流的峰值显着降低35.6 +/- 7.8％。这些发现表明，CRF降低了神经元的兴奋性，并降低了大鼠PVN NMU表型神经元在体外的T型Ca2+电流。 （c）2012年Elsevier Ireland Ltd.保留所有权利。
In the present study, we examined the effects of corticotrophin-releasing factor (CRF) on neuromedin U (NMU) mRNA-expressing neurons in the rat paraventricular nucleus (PVN) by whole-cell patch-clamp recordings and single-cell reverse transcription-multiplex polymerase chain reaction (single-cell RT-mPCR) techniques. In total, of 116 PVN putative parvocellular neurons screened for NMU mRNA, 14.7% (17/116) of them expressed NMU mRNA. The electrophysiological properties observed in the NMU mRNA-expressing neurons were generation of a low-threshold Ca2+ spike (LTS) and robust low voltage-activated (T-type) Ca2+ currents. Under current-clamp conditions, CRF (100 nM) induced a reversible decrease in spike firing and significantly diminished the LTS in 88.2% (15/17) of NMU mRNA-expressing neurons. Extracellular application of 1 mu M alpha-helical CRF-(9-14) (alpha-hCRF), a selective CRF receptor antagonist, completely blocked the CRF-induced decrease in spike firing in the NMU mRNA-expressing neurons. Under voltage-clamp conditions, CRF (100 nM) significantly decreased the peak value of the T-type Ca2+ currents by 35.6 +/- 7.8%. These findings suggest that CRF decreases neuronal excitability and diminishes T-type Ca2+ currents in a population of rat PVN NMU phenotype neurons in vitro. (C) 2012 Elsevier Ireland Ltd. All rights reserved.