Rosso L, Peteri-Brunbäck B, Mienville J-M
CNRS-UMR 6548, Laboratoire de Physiologie Cellulaire et Moléculaire, Université de Nice-Sophia Antipolis, Nice, France.
J Neuroendocrinol. 2004 Apr;16(4):313-8. doi: 10.1111/j.0953-8194.2004.01160.x.
Physiological stimuli operative during, for example, dehydration or lactation, induce neurohypophysial astrocytes (pituicytes) to undergo reversible morphological changes, which in turn may modulate the release of vasopressin and oxytocin. To study the molecular mechanisms of this morphological plasticity, we used primary cultures of rat pituicytes. During stimulation with adenosine, pituicytes become stellate, which is characterized by a round, phase-bright soma and complex arborization, implying major cytoskeletal modifications. Following addition of vasopressin or oxytocin, stellate pituicytes revert to a flat shape. The effects of both hormones are mediated by V(1a) receptor activation, which also induces biphasic Ca(2+) (i) signals in pituicytes. Stellation reversal requires Ca(2+)-dependent activation of Cdc42, a small GTPase known to impact on the cytoskeleton. V(1a) receptor activation by vasopressin or oxytocin also stimulates [(3)H]taurine efflux from cultured pituicytes. As taurine inhibits vasopressin output from neurohypophysial terminals, we postulate a negative-feedback mechanism whereby secreted vasopressin limits its own availability. This stop signal might be reinforced by shape changes elicited by vasopressin in pituicytes. These results support the concept that, during specific physiological states, pituicyte V(1a) receptor activation modulates the release of neurohypophysial hormones.
例如，在脱水或哺乳期间起作用的生理刺激会诱导神经垂体星形胶质细胞（垂体细胞）发生可逆的形态变化，这反过来可能会调节血管加压素和催产素的释放。为了研究这种形态可塑性的分子机制，我们使用了大鼠垂体细胞的原代培养物。在用腺苷刺激期间，垂体细胞变成星状，其特征是圆形、明亮的胞体和复杂的分支，这意味着细胞骨架发生了重大改变。加入血管加压素或催产素后，星状垂体细胞恢复为扁平形状。两种激素的作用均由V(1a)受体激活介导，这也会在垂体细胞中诱导双相Ca(2+)（i）信号。星状逆转需要Cdc42的Ca(2+)依赖性激活，Cdc42是一种已知会影响细胞骨架的小GTP酶。血管加压素或催产素对V(1a)受体的激活也会刺激培养的垂体细胞中[(3)H]牛磺酸的外流。由于牛磺酸会抑制神经垂体终末释放血管加压素，我们推测存在一种负反馈机制，即分泌的血管加压素会限制其自身的可用性。这种停止信号可能会因血管加压素在垂体细胞中引起的形状变化而得到加强。这些结果支持这样一种观点，即在特定生理状态下，垂体细胞V(1a)受体的激活会调节神经垂体激素的释放。
