| Autor: |
Giniatullin, R A, Khazipov, R N, Vyskocil, F |
| Zdroj: |
Journal of Physiology; July 1993, Vol. 466 Issue: 1 p95-103, 9p |
| Abstrakt: |
1. The relationship between quantal content and prolongation of endplate currents (EPC) was studied in the frog sartorius with intact synaptic acetylcholinesterase. 2. The prolongation of EPC was more pronounced in endplates with a higher quantal content both before and after potentiation of quantal release by 4‐aminopyridine (4‐AP). When the quantal content of EPC was lowered, either by high Mg2+ or repetitive stimulation, the EPC decay constant was reduced. 3. A certain critical value of about 120 quanta per nerve impulse was found, at which point the decay of EPC remained constant even through the quantal content was reduced further. 4. The reduction in both density and number of postsynaptic receptors, produced by alpha‐bungarotoxin and (+)‐tubocurarine led to a profound reduction in EPC decay during the progressive fall in EPC amplitude in both 4‐AP‐treated and ‐untreated endplates. Both drugs are known to produce a shortening of EPC in anti‐cholinesterase (anti‐ChE)‐treated muscles, due to a decrease in receptor density and less frequent repetitive binding of ACh. 5. It is assumed that the prolongation of multiquantal EPC is caused by an increased ACh concentration near the receptors, which may provide the opportunity for repetitive binding even with full cholinesterase activity. The critical quantum content of about 120 might be the number of quanta at which the probability of multiple release at single active zones is increased above zero. |
| Databáze: |
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