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首页> 外文期刊>Life sciences >Dual regulation of heat-activated K+ channel in rat DRG neurons via alpha(1) and beta adrenergic receptors.
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Dual regulation of heat-activated K+ channel in rat DRG neurons via alpha(1) and beta adrenergic receptors.

机译：通过α（1）和β肾上腺素受体对大鼠DRG神经元中的热激活K +通道的双重调节。

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AIMS: The present study aimed at understanding regulation of heat-activated K+ channels expressed in DRG neurons. MAIN METHODS: Whole-cell patches were made from cultured rat dorsal root ganglion (DRG) neurons and heat-activated currents were monitored. KEY FINDINGS: A temperature rise from 25 to 45 degrees C generated outward currents with the current/voltage relation revealing a reversal potential of approximately -90 mV, that are inhibited by the K+ channel blockers, Ba2+ and tetraethylammonium, indicating that heat activates K+ channels expressed in DRG neurons. Heat-activated K+ channel currents here was depressed by noradrenaline, and a similar effect was obtained with cirazoline, an agonist of alpha1 adrenergic receptors linked to G(q) protein involving PKC activation, and isoproterenol, an agonist of beta adrenergic receptors linked to G(s) protein involving PKA activation, but not UK14304, an agonist of alpha2 adrenergic receptors linked to G(i) protein. The noradrenaline action was prevented by GF109203X, a PKC inhibitor, or H-89, a PKA inhibitor, and a complete inhibition was obtained with co-treatment with GF109203X and H-89. PMA, a PKC activator, or forskolin, an activator of adenylate cyclase, on the other hand, reduced heat-activated outward currents and co-treatment with PMA and forskolin further attenuated the currents to an extent similar to that for noradrenaline. SIGNIFICANCE: The results of the present study show that heat-activated K+ channel currents in DRG neurons are inhibited by both PKC and PKA as mediated via alpha1 and beta adrenergic receptors, respectively. This may represent a new insight into regulation of thermosensation via a noradrenergic pathway.
机译：目的：本研究旨在了解DRG神经元中表达的热激活K +通道的调节。主要方法：从培养的大鼠背根神经节（DRG）神经元制作全细胞膜片，并监测热激活电流。主要发现：温度从25摄氏度升高到45摄氏度，产生向外电流，电流/电压关系显示出约-90 mV的逆转电位，这被K +通道阻滞剂Ba2 +和四乙铵抑制，表明热量激活了K +通道在DRG神经元中表达。去甲肾上腺素抑制了热激活的K +通道电流，并通过与连接到PKC活化的G（q）蛋白的α1肾上腺素受体激动剂cirazoline和连接到G的β肾上腺素受体激动剂异丙肾上腺素获得了类似的效果。 （s）涉及PKA激活的蛋白质，但不涉及UK14304，UK14304是与G（i）蛋白质相连的α2肾上腺素能受体的激动剂。去甲肾上腺素的作用被PKC抑制剂GF109203X或PKA抑制剂H-89阻止，并且通过与GF109203X和H-89共同处理获得了完全的抑制作用。另一方面，PKA激活剂PMA或腺苷酸环化酶激活剂Forskolin减少了热激活的向外电流，与PMA和Forskolin共同处理进一步减弱了电流，其程度类似于去甲肾上腺素。意义：本研究的结果表明，DRG神经元中的热激活K +通道电流分别受α1和β肾上腺素受体介导的PKC和PKA抑制。这可能代表了通过去甲肾上腺素途径对热敏调节的新见解。

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