ATP released together with acetylcholine as the mediator of neuromuscular depression at frog motor nerve endings.

摘要: 1. The hypothesis that ATP released by presynaptic stimulation is hydrolysed to adenosine and mediates prejunctional neuromuscular depression was tested at vertebrate junctions. Electrophysiological recordings of evoked acetylcholine (ACh) release perineural ionic currents motor nerve endings were made using the frog cutaneous pectoris nerve-muscle preparation. Either tubocurarine or alpha-bungarotoxin used block muscle contractions. 2. alpha,beta-methylene ADP (which inhibits ecto-5'nucleotidases thus prevents degradation adenosine) selective receptor antagonists (8-cyclo-pentyl alkyl xanthines) prevented inhibitory effects exogenous on ACh in response low-frequency stimulation. These results confirm earlier findings must be inhibit release. 3. presence completely repetitive high-frequency (0.5-1 Hz). alpha,beta-Methylene had no effect secretion under conditions where well maintained (low-frequency stimulation, 0.05 4. Selective eliminated produced (1.0 Hz) but low frequencies (0.05 5. Exogenous deaminase (5 i.u. ml-1), which degrades its inactive nucleoside inosine, also significant too produce depression. 6. During maximal depression, 2-chloroadenosine, an agonist, occluded. 7. calcium-sensitive component perineurial terminal did not change during application deaminase, suggesting this species associated with changes Ca2+ currents. 8. suggest that, these experiments, endogenous ATP, after hydrolysis adenosine, causes This occurs a site distal locus entry frog.