I think you should start from methods of RRP measure. If RRP is the average number of vesicles released at very rare stimulus than we can conclude high variability of RRP size. Consequently the calcium concentration does effectively affects the RRP size. On the other hand you can assess the RRP size by linear approximation of initial part of the quantum content curve during high-frequency stimulation. In this case the size of the RRP seems to be more constant and to increase its size you have to induce nerve endings growth. I have a couple paper related to this question: 1) The vesicle cycle in motor nerve endings of the mouse diaphragm; 2) Experimental and modeling investigation of the mechanism of synaptic vesicles recycling

Firstly, thank you for your response. We do not have any problem measuring the RRP size. Generally, we use high-frequency train stimuli to obtain RRP. I just want to learn the main source leading to increment in the RRP size. What is the relationship between Ca2+ increment and the RRP size or between the number of active boutons and RRP size? or if it is so, what is the strength of the relationship among them?

Actually I believe that the RRP size is just a result of the instant probability of vesicle exocytosis. If so, current Ca2+ concentration strongly impact RRP size by mean docking molecular machinery (SNAP-25, syntaxin, synaptotagmin and so on). Increasing the concentration of Ca2+ leads to more probable activation of Ca-sensors and more reliable exocytosis.

Synaptic terminals can increase the release of the number of vesicles per action potential after repetitive stimulation. Release can be enhanced if the release probability (pr) has become higher or if the number of vesicles available for release, the so-called readily releasable pool (rrp), is larger.