Bournaud R, Hidalgo J, Yu H, Girard E, Shimahara T
Laboratoire de Neurobiologie Cellulaire et Moléculaire, Institut Alfred Fessard CNRS UPR 9040, Avenue de la Terrasse, 91198 Gif sur Yvette Cedex, France.
Pflugers Arch. 2007 Apr;454(1):83-92. doi: 10.1007/s00424-006-0185-z. Epub 2006 Dec 13.
The adrenal medulla chromaffin cells (AMCs) secrete catecholamines in response to various types of stress. We examined the hypoxia-sensitivity of catecholamine secretion by rat foetal chromaffin cells in which the innervation by the splanchnic nerve is not established. The experiments were performed in primary cultured cells from two different ages of foetuses (F15 and F19). Membrane potential of AMCs was monitored with the patch clamp technique, and the catecholamine secretion was detected by amperometry. We found that: (1) AMCs from F19 foetuses showed hypoxia-induced catecholamine release. (2) This hypoxia-induced secretion is produced by membrane depolarization generated by an inhibition of Ca(2+)-activated K(+) current [I (K(Ca))] current. (3) Chromaffin precursor cells from F15 foetuses secrete catecholamine. The quantal release is calcium-dependent, but the size of the quantum is reduced. (4) In the precursor cells, a hypoxia-induced membrane hyperpolarization is originated by an ATP-sensitive K(+) current [I (K(ATP))] activation. (5) During the prenatal period, at F15, the percentage of the total outward current for I (K(ATP)) and I (K(Ca)) was 50 and 29.5%, respectively, whereas at F19, I (K(ATP)) is reduced to 14%, and I (K(Ca)) became 64% of the total current. We conclude that before birth, the age-dependent hypoxia response of chromaffin cells is modulated by the functional activity of K(ATP) and K(Ca) channels.
肾上腺髓质嗜铬细胞（AMCs）会因应各种类型的应激而分泌儿茶酚胺。我们研究了未建立内脏神经支配的大鼠胎儿嗜铬细胞儿茶酚胺分泌的缺氧敏感性。实验在来自两个不同胎龄（F15和F19）胎儿的原代培养细胞中进行。用膜片钳技术监测AMCs的膜电位，并用安培法检测儿茶酚胺分泌。我们发现：（1）来自F19胎儿的AMCs表现出缺氧诱导的儿茶酚胺释放。（2）这种缺氧诱导的分泌是由抑制钙激活钾电流[I（K（Ca））]电流产生的膜去极化所引起。（3）来自F15胎儿的嗜铬前体细胞分泌儿茶酚胺。量子释放依赖于钙，但量子大小减小。（4）在前体细胞中，缺氧诱导的膜超极化是由ATP敏感性钾电流[I（K（ATP））]激活引起的。（5）在产前阶段，F15时，I（K（ATP））和I（K（Ca））占总外向电流的百分比分别为50%和29.5%，而在F19时，I（K（ATP））降至14%，I（K（Ca））占总电流的64%。我们得出结论，在出生前，嗜铬细胞的年龄依赖性缺氧反应受K（ATP）和K（Ca）通道的功能活性调节。
