Lovell P V, McCobb D P
Department of Neurobiology and Behavior, Cornell University, Ithaca, New York 14853, USA.
J Neurosci. 2001 May 15;21(10):3429-42. doi: 10.1523/JNEUROSCI.21-10-03429.2001.
The discovery that the hypothalamic-pituitary-adrenocortical (HPA) endocrine stress axis controls an alternative splicing decision in chromaffin Slo-encoded BK (big potassium) channels raised the possibility that activation of the HPA could serve as a mechanism to tune the intrinsic electrical properties of epinephrine-secreting adrenal chromaffin cells. To test this, we compared BK functional properties and cell excitability in chromaffin cells from normal and hypophysectomized (pituitary-ablated) rats. Hypophysectomy was found to alter the voltage dependence and kinetics of BK gating, making channels less accessible for activation from rest. Perforated-patch recordings revealed changes in action potential waveform and repetitive firing properties. The maximum number of spikes that could be elicited with a 2 sec depolarizing current pulse was reduced by approximately 50% by hypophysectomy. The results indicate that pituitary hormones can adapt the mechanics of adrenal catecholamine release by tailoring BK channel function.
下丘脑 - 垂体 - 肾上腺皮质(HPA)内分泌应激轴控制嗜铬细胞中Slo编码的大钾(BK)通道的可变剪接决定这一发现,提出了HPA轴激活可能作为调节分泌肾上腺素的肾上腺嗜铬细胞内在电特性的一种机制的可能性。为了验证这一点,我们比较了正常大鼠和垂体切除(垂体消融)大鼠的嗜铬细胞中BK的功能特性和细胞兴奋性。结果发现垂体切除会改变BK门控的电压依赖性和动力学,使通道从静息状态激活的可能性降低。穿孔膜片钳记录揭示了动作电位波形和重复放电特性的变化。垂体切除使2秒去极化电流脉冲引发的最大尖峰数量减少了约50%。结果表明,垂体激素可通过调整BK通道功能来适应肾上腺儿茶酚胺释放的机制。