Diadenosine pentaphosphate

Diadenosine pentaphosphate is an endogenous generated diadenosine polyphosphate, possessing the dual identities of intracellular alarm signal and extracellular signaling molecule. Diadenosine pentaphosphate regulates calcium signaling in the nervous, cardiac and peripheral sensory systems by activating P2X1/P2X3/P2Y receptor and RyR2 channels (EC₅₀ = 140 μM). Ap5A can be used in studies related to intracellular calcium release channels, cardiovascular diseases and nociception (pain)^{[1][3][2][4][5]}. In Vitro:Ap5A (100 μM) elevates the intracellular calcium level of cultured human fetal astrocytes to 980 nM via P2 purinergic receptor-mediated extracellular calcium influx, as well as calcium release from IP₃-sensitive and ryanodine-sensitive intracellular calcium stores^[1].
Ap5A (100 μM; 5 sec) increases the production of IP₃ in cultured human fetal astrocytes by approximately 2-fold^[1].
Ap5A (10 μM) activates the I_KACh current in isolated guinea pig atrial myocytes by stimulating P1 receptors^[2].
Ap5A (100 μM) induces local, transient increases in intracellular calcium in distal dendrites and dendritic growth cones of E18 mouse hippocampal neurons cultured in vitro, with no effect on calcium levels in axons or somatodendritic regions^[5].
Ap5A (100 μM; 72 h) exerts a negative regulatory effect on dendrite growth and quantity in E18 mouse hippocampal neurons cultured in vitro (in phenol red-free medium). After treatment with 100 μM for 72 h, it reduces the total dendrite length by 28.7% and the number of dendrites by 28.1%, but has no effect on axon length^[5].
Ap5A (100 μM) - Overexpression of P2X1 mimics Ap5A-induced reductions in dendritic length and number in cultured E18 mouse hippocampal neurons in vitro, whereas P2X1-knockdown shRNA reverses Ap5A-induced reduction in dendritic number but fails to reverse the reduction in dendritic length^[5].