Kwiecien R, Hammond C
Dynamique des Systèmes Neuroendocriniens, INSERM U159, Paris, France.
Neuroendocrinology. 1998 Sep;68(3):135-51. doi: 10.1159/000054360.
Most electrical and ionic properties of anterior pituitary cells are common to all pituitary cell types; only gonadotropes exhibit a few cell specific features. Under basal conditions, the majority of pituitary cells in vitro, irrespective of their cell type, display spontaneous action potentials and [Ca2+]i transients that result from rhythmic Ca2+ entry through L-type Ca2+ channels. The main function of these action potentials is to maintain cells in a readily activable responsive state. We propose to call this state a 'pacemaker mode', since it persists in the absence of extrinsic stimulation. When challenged by hypothalamic releasing hormones, cells exhibit two distinct response patterns: amplification of pacemaker activity or shift to internal Ca2+ release mode. In the internal Ca2+ release mode, [Ca2+]i oscillations are not initiated by entry of external Ca2+, but by release of Ca2+ from intracellular stores. In somatotropes and corticotropes, GHRH or CRH triggers the pacemaker mode in silent cells and amplifies it in spontaneously active cells. In contrast, in gonadotropes GnRH activates the internal Ca2+ release mode in silent cells and switches already active cells from the pacemaker to the internal Ca2+ release mode. Interestingly, homologous normal and tumoral cells display the same type of activity in vitro, in the absence or presence of hypothalamic hormones. Pacemaker and internal Ca2+ release modes are likely to serve different purposes. Pacemaker activity allows long-lasting sequences of [Ca2+]i oscillations (and thus sustained periods of secretion) that stop under the influence of hypothalamic inhibitory peptides. In contrast, the time during which cells can maintain internal Ca2+ release mode depends upon the importance of intracellular Ca2+ stores. This mode is thus more adapted to trigger secretory peaks of large amplitude and short duration. On the basis of these observations, theoretical models of pituitary cell activity can be proposed.
垂体前叶细胞的大多数电学和离子特性为所有垂体细胞类型所共有；只有促性腺激素细胞表现出一些细胞特异性特征。在基础条件下，体外培养的大多数垂体细胞，无论其细胞类型如何，都会显示出自发动作电位和[Ca2+]i瞬变，这是由通过L型Ca2+通道的节律性Ca2+内流引起的。这些动作电位的主要功能是使细胞维持在易于激活的反应状态。我们建议将这种状态称为“起搏器模式”，因为它在没有外部刺激的情况下持续存在。当受到下丘脑释放激素的刺激时，细胞会表现出两种不同的反应模式：起搏器活动的放大或转变为内部Ca2+释放模式。在内部Ca2+释放模式下，[Ca2+]i振荡不是由外部Ca2+的内流引发，而是由细胞内储存的Ca2+释放引发。在生长激素细胞和促肾上腺皮质激素细胞中，生长激素释放激素（GHRH）或促肾上腺皮质激素释放激素（CRH）会在静息细胞中触发起搏器模式，并在自发活动的细胞中放大该模式。相反，在促性腺激素细胞中，促性腺激素释放激素（GnRH）会在静息细胞中激活内部Ca2+释放模式，并将已经活跃的细胞从起搏器模式切换到内部Ca2+释放模式。有趣的是，同源的正常细胞和肿瘤细胞在体外，无论是否存在下丘脑激素，都表现出相同类型的活动。起搏器模式和内部Ca2+释放模式可能具有不同的目的。起搏器活动允许[Ca2+]i振荡的持久序列（从而实现持续的分泌期），这些振荡在下丘脑抑制性肽的影响下停止。相反，细胞能够维持内部Ca2+释放模式的时间取决于细胞内Ca2+储存的量。因此，这种模式更适合触发大振幅、短持续时间的分泌高峰。基于这些观察结果，可以提出垂体细胞活动的理论模型。
