TY - JOUR
T1 - A study of tetanic and post‐tetanic potentiation of miniature end‐plate potentials at the frog neuromuscular junction.
AU - Lev‐Tov, A.
AU - Rahamimoff, R.
PY - 1980/12/1
Y1 - 1980/12/1
N2 - 1. The involvement of calcium sodium, potassium and magnesium in tetanic and post‐tetanic potentiation of miniature end‐plate potential frequency was examined at the frog neuromuscular junction using conventional electrophysiological techniques. 2. Tetanic potentiation is larger in calcium containing solutions, than in solutions which generate reversed electrochemical gradient for calcium during nerve activity. 3. Tetanic potentiation increases with stimulation frequency and duration, under both inward and reversed electrochemical gradient for calcium conditions. This indicates that factors, other than calcium entry, participate in tetanic potentiation. 4. Addition of the potassium conductance blocking agent, 3‐aminopyridine (5 mM), increases tetanic potentiation in calcium containing media, while depressing it under reversed calcium gradient. 5. Electronic depolarization of the nerve terminal in tetrodotoxin‐containing Ringer solution, produces tetanic potentiation under inward gradient, but fails to do so under reversed gradient. This indicates that the entry of sodium ions participates in the generation of tetanic potentiation. 6. Addition of magnesium ions suppresses tetanic potentiation in calcium containing solution, but increases tetanic potentiation under reversed gradient. 7. The results are explained by the hypothesis that calcium entry and intracellular calcium translocation participate in the generation of tetanic potentiation. 8. Both the fast and the slow components (augmentation and potentiation respectively) of post‐tetanic potentiation increase in duration, with increase in the tetanic stimulation rate. 9. The decay of post‐tetanic potentiation increases: when [Ca]o is elevated by ionophoretic application during the decay phase only, when ouabain is present in the medium or when [Mg]o is elevated. These finding suggest that calcium, sodium and possibly magnesium take part in post‐tetanic potentiation.
AB - 1. The involvement of calcium sodium, potassium and magnesium in tetanic and post‐tetanic potentiation of miniature end‐plate potential frequency was examined at the frog neuromuscular junction using conventional electrophysiological techniques. 2. Tetanic potentiation is larger in calcium containing solutions, than in solutions which generate reversed electrochemical gradient for calcium during nerve activity. 3. Tetanic potentiation increases with stimulation frequency and duration, under both inward and reversed electrochemical gradient for calcium conditions. This indicates that factors, other than calcium entry, participate in tetanic potentiation. 4. Addition of the potassium conductance blocking agent, 3‐aminopyridine (5 mM), increases tetanic potentiation in calcium containing media, while depressing it under reversed calcium gradient. 5. Electronic depolarization of the nerve terminal in tetrodotoxin‐containing Ringer solution, produces tetanic potentiation under inward gradient, but fails to do so under reversed gradient. This indicates that the entry of sodium ions participates in the generation of tetanic potentiation. 6. Addition of magnesium ions suppresses tetanic potentiation in calcium containing solution, but increases tetanic potentiation under reversed gradient. 7. The results are explained by the hypothesis that calcium entry and intracellular calcium translocation participate in the generation of tetanic potentiation. 8. Both the fast and the slow components (augmentation and potentiation respectively) of post‐tetanic potentiation increase in duration, with increase in the tetanic stimulation rate. 9. The decay of post‐tetanic potentiation increases: when [Ca]o is elevated by ionophoretic application during the decay phase only, when ouabain is present in the medium or when [Mg]o is elevated. These finding suggest that calcium, sodium and possibly magnesium take part in post‐tetanic potentiation.
UR - http://www.scopus.com/inward/record.url?scp=0019225804&partnerID=8YFLogxK
U2 - 10.1113/jphysiol.1980.sp013507
DO - 10.1113/jphysiol.1980.sp013507
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C2 - 6973021
AN - SCOPUS:0019225804
SN - 0022-3751
VL - 309
SP - 247
EP - 273
JO - Journal of Physiology
JF - Journal of Physiology
IS - 1
ER -