Do ryanodine receptors regulate transmitter release at the neuromuscular junction of rat?

It has been suggested that calcium that is stored in nerve terminals can be released via activation of ryanodine receptors and this source of calcium could serve to modulate evoked transmitter release. Calcium influx via voltage dependent calcium channels could lead to calcium induced calcium release via ryanodine receptors in neuronal tissue. This additional source of calcium could contribute to the total calcium that is available for transmitter release or it could result in having a negative feedback action on calcium influx and transmitter release. We examined the effect of blocking and activating the ryanodine receptors on quantal transmitter release at the rat neuromuscular junction. Intracellular recording techniques were used to monitor end-plate potentials and miniature end-plate potentials. The data supports the view that intracellular calcium released via ryanodine receptors suppresses calcium influx leading to depressed quantal release.