Figure 10.

A schematic model for Sr²⁺-induced [Ca²⁺]_cy spikes in E. viridis. Sr²⁺ enters the cell via Ca²⁺ channels in the plasma membrane that are competitively blocked by Gd³⁺ or La³⁺. Most of the Sr²⁺ taken up into the cell is compartmentalized into the vacuole. At steady state, the same amount of Sr²⁺ (and Ca²⁺) that enters the cell is transported out of the cell by plasma membrane Ca²⁺-ATPases. The Ca²⁺-ATPases that pump Sr²⁺ (and Ca²⁺) into the vacuole or out of the cell are not blocked by DBHQ or CPA. Inside the cell Sr²⁺ induces a Ca²⁺-release from the ER. The ER Ca²⁺ channel is inhibited by either ruthenium red (RR) or ryanodine (Ry), pointing to a ryanodine/cADPR-like Ca²⁺ channel. The rapid increase in [Ca²⁺]_cy is compensated for by Ca²⁺-ATPases of internal Ca²⁺ stores and the plasma membrane. The ER is refilled by Ca²⁺-ATPases that are blocked by DBHQ or CPA. The [Ca²⁺]_cy spike causes the opening of plasma membrane K⁺ channels, resulting in a transient hyperpolarization. This K⁺ channel is known to be blocked by Ba²⁺ or TEA (Köhler et al., 1983; Thaler et al., 1989).