FIGURE 10.

Proposed mechanisms initiated by LPI at the sarcolemma or within the neonatal ventricular cardiomyocyte via GPR55. LPI activates GPR55 located on the membrane of endolysosomes (Endo-Lys) to promote NAADP-dependent Ca²⁺ release from these organelles, which further induces CICR via RyRs located at the SR and converging to membrane hyperpolarization (top, blue). GPR55 stimulation at the sarcoplasmic membrane results, on one hand, in Ca²⁺ entry through LTCCs and, on the other, in IP₃-dependent Ca²⁺ release from the intracellular stores, a signal further amplified by CICR via RyRs. Independently of Ca²⁺ signaling, GPR55 activation results in membrane depolarization (bottom, red).