Cholinoreceptors of early (preneural) sea urchin embryos.

Agonists of nicotinic cholinoreceptors (n-AChR) and 1-acetyl-4-methylpiperazine (100 microM) 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.