Cholinoreceptors of early (preneural) sea urchin embryos

被引：8

作者：

Buznikov G.A. ^{[1
]}

Rakich L. ^{[2
,3
]}

机构：

[1] N. K. Kol'tsov Institute of Developmental Biology, Russian Academy of Sciences, 117808 Moscow

来源：

Neuroscience and Behavioral Physiology | 2000年 / 30卷 / 1期

基金：

俄罗斯基础研究基金会;

关键词：

Cholinoreceptors; Early embryos; Oocytes; Protein kinase C activators;

D O I：

10.1007/BF02461392

中图分类号：

学科分类号：

摘要：

Agonists of nicotinic cholinoreceptors (n-AChR) and 1-acetyl-4-methylpiperazine (100 μM) had no effect on early embryogenesis in sea urchins, while in the presence of phorbol-12-myristate-13-acetate (PMA) and various other protein kinase C activators, these agents induced rapid lysis of oocytes or early embryos, as a result of calcium shock. Many n-AChR ligands which do not penetrate into the cytoplasm (not being antagonists of muscarinic cholinoreceptors) protected against this cytotoxic effect. In the presence of PMA, acetylcholine and carbachol had actions which were much weaker than those of nicotine, while muscarine was completely inactive in these conditions. Thus, the surfaces of sea urchin oocytes and early embryos bear receptor structures, presumably n-AChR, which are functionally linked with second messengers which are endogenous protein kinase C activators.

引用

页码：53 / 62

页数：9

共 36 条

[21] Khiroug L., Giniatullin R., Sokolova E., Talanova M., Nistri A., Imaging of intracellular calcium during desensitization of nicotinic acetylcholine receptors of rat chromaffin cells, Brit. J. Pharmacol., 122, 7, pp. 1323-1332, (1997)
[22] Lauder J.M., Neurotransmitters as growth regulatory signals: Role of receptors and second messengers, Trends Neurosci., 16, 6, pp. 233-240, (1993)
[23] Letz B., Schomerus C., Maronde E., Korf H.W., Korbmacher C., Stimulation of a nicotinic ACh receptor causes depolarization and activation of L-type Ca<sup>2+</sup> channels in rat pinealocytes, J. Physiol. (London), 499, 2, pp. 329-340, (1997)
[24] Limatola C., Plama E., Mileo A.M., Eusebi F., Phorbol ester modulation of both delta-mutant and subunit-omitted nicotinic receptors expressed in Xenopus oocytes, Brain Res., 742, 1-2, pp. 172-176, (1996)
[25] Lukas R., Diversity and patterns of regulation of nicotinic receptor subtypes, Ann. N.Y. Acad. Sci., 757, pp. 153-168, (1995)
[26] Marley P.D., Thomson K.A., Inhibition of nicotinic responses of bovine adrenal chromaffin cells by the protein kinase C inhibitor, Ro 31-8220, Brit. J. Pharmacol., 119, 2, pp. 416-422, (1996)
[27] Mclane K.E., Dunn S.J.M., Manfredi A.A., Contitronconi B.M., Raftery M.A., The nicotinic acetylcholine receptor as a model for a superfamily of ligand-gated ion channel proteins, Protein Engineering and Design, pp. 289-352, (1996)
[28] Olds J.L., Favit A., Nelson T., Ascoli G., Gerstein A., Cameron M., Cameron L., Lester D.S., Rakow T., De Barry J., Yoshioka T., Freyberg Z., Baru J., Alkon D.L., Imaging protein kinase C activation in living sea urchin eggs after fertilization, Dev. Biol., 172, 2, pp. 675-682, (1995)
[29] Quik M., Philie J., Choremis J., Modulation of alpha 7 nicotinic receptor-mediated calcium influx by nicotinic agonists, Moll. Pharmacol., 51, 3, pp. 499-506, (1997)
[30] Silver R.B., Calcium, BOBs, QEDs, microdomains, and a cellular decision. Control of mitotic cell division in sand dollar blastomeres, Cell Calcium, 20, 1, pp. 161-179, (1996)

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