Pan Zhizhong Z
Department of Symptom Research, University of Texas-MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
J Physiol. 2003 May 1;548(Pt 3):765-75. doi: 10.1113/jphysiol.2002.037622. Epub 2003 Mar 21.
The hyperpolarization-activated current (Ih) is important in the control of resting membrane potential, in the regulation of network firing pattern and in the modulation of presynaptic transmitter release in central neurons. Recent studies on native and cloned Ih channels have demonstrated that the Ih channel is commonly modulated by cAMP through a positive shift in its voltage dependence without a change in its maximum current. The present study demonstrates that activation of kappa-opioid receptors enhances Ih by increasing its maximum current in brainstem neurons in the nucleus raphe magnus. Agents that interfere with the release of intracellular calcium from calcium stores altered the maximum Ih and significantly attenuated the kappa-receptor-mediated enhancement of Ih. These results suggest that kappa-opioid receptors enhance the maximum Ih by mobilizing intracellular calcium from calcium stores. This provides a physiological function for kappa-receptor-stimulated calcium release and may suggest another Ih-regulating mechanism by intracellular calcium in central neurons.
超极化激活电流（Ih）在控制静息膜电位、调节网络放电模式以及调节中枢神经元突触前递质释放方面具有重要作用。最近对天然和克隆的Ih通道的研究表明，Ih通道通常通过其电压依赖性的正向偏移而被cAMP调节，而其最大电流不变。本研究表明，κ-阿片受体的激活通过增加中缝大核脑干神经元的最大电流来增强Ih。干扰细胞内钙从钙库释放的药物改变了最大Ih，并显著减弱了κ-受体介导的Ih增强。这些结果表明，κ-阿片受体通过从钙库动员细胞内钙来增强最大Ih。这为κ-受体刺激的钙释放提供了一种生理功能，并可能提示中枢神经元中细胞内钙的另一种Ih调节机制。
