The second messenger cAMP regulates many diverse cellular functions.$$ In the intestinal lumen, cAMP is responsible for maintaining electrolyte and water balance.$$ Certain bacterial toxins, including one produced by Vibrio cholera, can upset the levels of cAMP because Gs remains in an active state ultimately leading to fatal dehydration and is called Vibrio cholera toxin $($CTX$).$

Given what you know about the mechanism of Vibrio cholera toxin, how would intracellular cAMP and PKA concentrations would change, as a function of time, for normal intestinal epithelial cells $($normal cells$)$ treated with a GPCR agonist to result in activation of the Galpha s protein subunit, as compared with cholera$-$toxin treated cells $($CT cells$)$ stimulated with the same GPCR agonist?

Choose all that apply:$$