inositol trisphosphate
IP3 is the messenger that opens the cell's internal calcium reservoir. Picture the endoplasmic reticulum as a dam holding back a store of calcium; IP3 is the key that opens the floodgates so calcium pours into the cytoplasm.
It is generated when phospholipase C cleaves the membrane lipid PIP2, releasing IP3 (water-soluble) and diacylglycerol (membrane-bound). IP3 diffuses through the cytosol to IP3 receptors — which are calcium channels on the endoplasmic reticulum — and binds them, letting stored calcium escape and sharply raising intracellular calcium. That calcium then drives contraction, secretion, and many enzymes, and also helps activate protein kinase C alongside DAG.
IP3 is deliberately short-lived: it is rapidly dephosphorylated, which terminates the calcium release and lets the signal be pulsed or oscillated rather than left switched on. This pathway is the engine behind Gq-coupled responses, so drugs that block upstream Gq receptors — alpha-1 blockers, AT1 blockers, M3 antagonists — indirectly silence the IP3-calcium signal.
Acetylcholine on M3 receptors in a salivary gland triggers phospholipase C; the resulting IP3 releases calcium from internal stores, and the cell secretes saliva.
IP3 turns a receptor signal into a burst of internal calcium.