Mechanism of (-)clausenamide induced calcium transient in primary culture of rat cortical neurons.

(-)clausenamide is a compound isolated from Clausena lansium (lour) Skeel with nootropic effects. At the present study, we investigated the clausenamide induced Ca2+ signaling in primary cultures of rat cortical neurons by using laser confocal microscopy. The mean amplitude of (-)clausenamide (1 microM) induced Ca2+ transient was similar in extracellular solution with or without calcium; and (-)clausenamide failed to trigger calcium transient after treatment with endoplasmic reticulum Ca2+ pumps inhibitor BHQ to exhaust intracellular Ca2+ stores. This result suggested that the primary source of (-)clausenamide induced Ca2+ transient was from internal stores. Application of IP3 receptor inhibitor MgCl2 and PLC-gamma inhibitor U73122 suppressed (-)clausenamide induced Ca2+ transient, suggesting that the major source of (-)clausenamide induced Ca2+ transient was from IP3 receptor pathway. We also found that mitochondria were involved in (-)clausenamide triggered Ca2+ transient. The distinctive spatial and temporal characteristic of (-)clausenamide induced Ca2+ transient may play an important role in its action.