Expression of a functional hyperpolarization-activated current (Ih) in the mouse nucleus reticularis thalami.
Expression of a functional hyperpolarization-activated current (Ih) in the mouse nucleus reticularis thalami.
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DOI：
10.1152/jn.00922.2005
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发表时间：
2006-05
影响因子：
2.5
通讯作者：
Y. Rateau;N. Ropert
中科院分区：
文献类型：
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作者：
Y. Rateau;N. Ropert
丘脑网状核(NRT)的GABA能神经元表达2型超极化激活的cAMP敏感(HCN2)亚单位，但令人惊讶的是，据报道它们缺乏由该亚单位携带的超极化激活(Ih)电流。在新生小鼠和幼年小鼠的丘脑皮质脑片(P6-P23)的电压钳记录中，我们证明，在1 mM的Ba2+存在下，NRT神经元表现出一种缓慢的超极化激活的内向电流，这表明Ih的存在，但在对照条件下被K+泄漏电流所掩盖。我们通过研究超极化激活电流在Ba2+存在下的生理和药理学特征来研究超极化激活电流在NRT中的同一性。我们证明了它具有Ih的典型的电压和时间依赖的性质，它被Ih的两个阻滞剂铯和ZD7288所阻断，并且它被K+和Na+离子携带。我们还可以改变NRT中超极化激活电流的门控特性，方法是在移液管溶液中添加非水解性cAMP类似物。最后，利用电流钳记录，我们发现阻断超极化激活电流引起的超极化与NRT神经元R(In)的增加有关。总之，我们的结果表明，NRT神经元表达Ih的速度与同质HCN_2通道相似，并且NRT的Ih参与了正常情况下NRT神经元的兴奋性。
The GABAergic neurons of the nucleus reticularis thalami (nRT) express the type 2 hyperpolarization-activated cAMP-sensitive (HCN2) subunit mRNA, but surprisingly, they were reported to lack the hyperpolarization-activated (Ih) current carried by this subunit. Using the voltage-clamp recordings in the thalamocortical slice preparation of the newborn and juvenile mice (P6-P23), we demonstrate that, in the presence of 1 mM barium (Ba2+), the nRT neurons express a slow hyperpolarization-activated inward current, suggesting that the Ih is present but masked in control conditions by K+ leak currents. We investigate the identity of the hyperpolarization-activated current in the nRT by studying its physiological and pharmacological profile in presence of Ba2+. We show that it has voltage- and time-dependent properties typical of the Ih, that it is blocked by cesium and ZD7288, two blockers of the Ih, and that it is carried both by the K+ and Na+ ions. We could also alter the gating characteristics of the hyperpolarization-activated current in the nRT by adding a nonhydrolysable analogue of cAMP to the pipette solution. Finally, using the current-clamp recording, we showed that blocking the hyperpolarization-activated current induced an hyperpolarization correlated with an increase of the R(in) of the nRT neurons. In conclusion, our results demonstrate that the nRT neurons express the Ih with slow kinetics similar to those described for the homomeric HCN2 channels, and we show that the Ih of the nRT contributes to the excitability of the nRT neurons in normal conditions.