In situ calcium signaling no calcium sparks detected in rat myometrium

Controlled uterine smooth muscle activity is essential for our reproductive health. While we understand reasonably well the steps that produce contraction following a rise in intracellular [Ca], the mechanism controlling excitability and thus the rise of Ca, is less well understood. Here we examine the role of the internal Ca sore, the sarcoplasmic reticBlum (SR), and its relation to surface membrane ion channels. We show that despite having a well-developed SR, the rat uterus does not produce the elemental and local Ca signals, known as Ca sparks. This in turn has consequences for excitability, as the negative feedback loop between these Ca signals and Ca-activated K (BK) channels on the surface membrane is lost. This may be important for producing the powerful long-lasting contractions of the uterus required during labor.