TY - JOUR
T1 - Evoked phasic release in frog nerve terminals obtained after block of Ca2+ entry by Cd2+
AU - Dudel, J.
AU - Parnas, H.
AU - Parnas, I.
PY - 1991/9
Y1 - 1991/9
N2 - Cutaneous pectoris muscles of frogs were isolated, mounted in a chamber and superfused with Ringer's solution. With a macro-patch-clamp electrode [5] placed on a section of a motor nerve terminal, quantal synaptic currents were elicited by depolarizing pulses and recorded. The electorde tip and the section of the terminal recorded from were perfused rapidly by Ringer's solution alone or containing 20-500 μM Cd2+ to block Ca2+ inflow. Separate superfusion of the muscle and the rest of the terminal with normal or elevated Ca2+ Ringer's solution provided a sufficiently high resting Ca2+ concentration in the terminal even when Ca2+ inflow was blocked by Cd2+. The depolarization level of maximal Ca2+ inflow into the terminal was found by measuring maximal test pulse facilitation, Fc [6]. In control solution as well as in the case of Cd2+ block, the rate of phasic release after depolarizing pulses rose further when depolarization was increased past the level of Fc, and reached a saturation level which was maintained at estimated depolarizations up to +200 mV. Block of Ca2+ inflow by Cd2+ decreased release substantially, but did not suppress it. The depression of release was greater in the range of large Ca2+ inflow (around Fc) than for very large depolarizations. The time course of phasic release was unaltered by blockage of Ca2+inflow. It is concluded that Ca2+ inflow contributes to the promotion of evoked release only in the depolarization range in which Ca2+ inward current is large. When Ca2+ concentration in the terminal is sufficiently high, release can be evoked by depolarization in the absence of Ca2+ inflow, the voltage-dependent release factor, S, compensating to a great extent for the lack of Ca2+ inflow.
AB - Cutaneous pectoris muscles of frogs were isolated, mounted in a chamber and superfused with Ringer's solution. With a macro-patch-clamp electrode [5] placed on a section of a motor nerve terminal, quantal synaptic currents were elicited by depolarizing pulses and recorded. The electorde tip and the section of the terminal recorded from were perfused rapidly by Ringer's solution alone or containing 20-500 μM Cd2+ to block Ca2+ inflow. Separate superfusion of the muscle and the rest of the terminal with normal or elevated Ca2+ Ringer's solution provided a sufficiently high resting Ca2+ concentration in the terminal even when Ca2+ inflow was blocked by Cd2+. The depolarization level of maximal Ca2+ inflow into the terminal was found by measuring maximal test pulse facilitation, Fc [6]. In control solution as well as in the case of Cd2+ block, the rate of phasic release after depolarizing pulses rose further when depolarization was increased past the level of Fc, and reached a saturation level which was maintained at estimated depolarizations up to +200 mV. Block of Ca2+ inflow by Cd2+ decreased release substantially, but did not suppress it. The depression of release was greater in the range of large Ca2+ inflow (around Fc) than for very large depolarizations. The time course of phasic release was unaltered by blockage of Ca2+inflow. It is concluded that Ca2+ inflow contributes to the promotion of evoked release only in the depolarization range in which Ca2+ inward current is large. When Ca2+ concentration in the terminal is sufficiently high, release can be evoked by depolarization in the absence of Ca2+ inflow, the voltage-dependent release factor, S, compensating to a great extent for the lack of Ca2+ inflow.
KW - Ca Current blocked by Cd
KW - Ca inflow
KW - Depolarization controlled release
KW - Neuromuscular transmission
KW - Time course of release
UR - http://www.scopus.com/inward/record.url?scp=0025948549&partnerID=8YFLogxK
U2 - 10.1007/BF00373007
DO - 10.1007/BF00373007
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C2 - 1660129
AN - SCOPUS:0025948549
SN - 0031-6768
VL - 419
SP - 197
EP - 204
JO - Pflugers Archiv European Journal of Physiology
JF - Pflugers Archiv European Journal of Physiology
IS - 2
ER -