Schomerus C, Laedtke E, Korf H W
Dr. Senckenbergische Anatomie, Anatomisches Institut II, Johann Wolfgang Goethe-Universität Frankfurt, Theodor-Stern-Kai 7, 60590, Frankfurt/Main, Germany.
Brain Res. 1999 Jun 26;833(1):39-50. doi: 10.1016/s0006-8993(99)01533-4.
In the rat pineal gland, norepinephrine activates alpha1- and beta-adrenergic receptors and triggers melatonin production through an increase in the intracellular calcium concentration ([Ca2+]i) and stimulation of the cAMP/cAMP responsive element-binding protein (CREB) cascade. VIP and PACAP also elevate the intracellular cAMP level and promote melatonin formation. Finally, ACh antagonizes the norepinephrine-induced hormone synthesis via nicotinic acetylcholine receptors and subsequent activation of voltage-gated calcium channels. By immuno(cyto)chemical demonstration of phosphorylated CREB and calcium imaging we have investigated the temporal relationship between the maturation of these signaling pathways and the rhythmic onset of melatonin biosynthesis in developing rat pinealocytes. Norepinephrine-regulated calcium signaling and phosphorylation of CREB are already fully developed at birth, i.e., prior to ingrowth of the sympathetic innervation into the pineal parenchyma, and appear to develop in an innervation-independent manner. VIP- and PACAP-induced CREB phosphorylation is restricted to subpopulations of neonatal cells and thus also displays an adult pattern. Cholinergic calcium signaling exhibits a developmental switch within the first three postnatal weeks. In neonatal pinealocytes, acetylcholine elevates [Ca2+]i via muscarinic rather than nicotinic acetylcholine receptors. In the second postnatal week, pinealocytes gain responsiveness to nicotine and gradually lose responsiveness to muscarinic cholinergic stimuli. Voltage-gated calcium channels are absent in neonatal cells and develop during the first postnatal days. ACh-evoked cellular events may be diversified depending on the functional subclass of receptor that is present. The transient existence of muscarinic acetylcholine receptors and the subsequent switch to nicotinic receptors would permit ACh to elicit temporary effects in early pineal development.
在大鼠松果体中,去甲肾上腺素激活α1和β肾上腺素能受体,并通过增加细胞内钙浓度([Ca2+]i)和刺激cAMP/ cAMP反应元件结合蛋白(CREB)级联反应来触发褪黑素的产生。血管活性肠肽(VIP)和垂体腺苷酸环化酶激活肽(PACAP)也会提高细胞内cAMP水平并促进褪黑素的形成。最后,乙酰胆碱通过烟碱型乙酰胆碱受体和随后电压门控钙通道的激活来拮抗去甲肾上腺素诱导的激素合成。通过磷酸化CREB的免疫(细胞)化学证明和钙成像,我们研究了这些信号通路的成熟与发育中大鼠松果体细胞中褪黑素生物合成的节律性起始之间的时间关系。去甲肾上腺素调节的钙信号传导和CREB的磷酸化在出生时就已完全发育,即在交感神经支配长入松果实质之前,并且似乎以与神经支配无关的方式发育。VIP和PACAP诱导的CREB磷酸化仅限于新生细胞亚群,因此也呈现出成年模式。胆碱能钙信号在出生后的前三周内表现出发育转换。在新生松果体细胞中,乙酰胆碱通过毒蕈碱型而非烟碱型乙酰胆碱受体升高[Ca2+]i。在出生后的第二周,松果体细胞对尼古丁产生反应,并逐渐失去对毒蕈碱型胆碱能刺激的反应。新生细胞中不存在电压门控钙通道,其在出生后的头几天发育。根据存在的受体功能亚类,乙酰胆碱诱发的细胞事件可能会有所不同。毒蕈碱型乙酰胆碱受体的短暂存在以及随后向烟碱型受体的转换将使乙酰胆碱在松果体早期发育中产生暂时作用。