Serotonin and acetylcholine modulate the sensitivity of early sea urchin embryos to protein kinase C activators

Abstract The protein kinase C activators 1-oleoyl-2-acetyl-rac-glycerol (OAG) and phorbol 12-myristate 13-acetate (PMA) evoke similar developmental anomalies in early embryos of sea urchins, that is, block of cleavage divisions, formation of giant polyploid nuclei with nucleolus-like inclusions, damage of cortical microfilaments and extrusion of small cytoplasts (mini-cells). Protein kinase inhibitors belonging to two different chemical groups (derivatives of isoquinoline and naphthalene) protect the embryos against OAG and PMA action. Some of these inhibitors (H-7, H-8, and H-9) also weaken the effects of 5-HT antagonists. 5-HT weakens and acetylcholine (ACh) potentiates the developmental anomalies evoked by PMA and OAG. It is suggested that endogenous 5-HT and ACh of early sea urchin embryos are functionally coupled with second messenger systems acting through the regulation of protein kinase C activity.