Adenosine effects upon the spontaneous quantal transmitter release at the frog neuromuscular junction in the presence of protein kinase C-blocking and -activating agents

This paper gives experimental evidence involving protein kinase C (PKC) in the inhibitory effects of adenosine (ADO) upon the spontaneous transmitter release at the frog neuromuscular junction. In the presence of two PKC inhibitors — polymyxin B (5 × 10 −6 mol/l) and H-7 (10 −5 mol/l), both adenosine (5 × 10 −5 mol/l) and its stable analogue 1-PIA (5 × 10 −8 mol/l), significantly increased the rate of the release of acetylcholine quanta. Even when PKC was activated with OAG (5 × 10 −6 mol/l) or TPA (162 × 10 −9 mol/l) and quantal release was increased greatly, ADO still inhibited release. ADO deaminase increased the PKC-induced activation of the transmitter release significantly.