Modification of transmitter release by ions which prolong the presynaptic action potential

Abstract

1. The action of ions which increase the nerve spike duration at Ranvier's node has been studied at the neuromuscular junction of the frog. The duration of the presynaptic action potential is increased by UO2, Ni, Nz and TEA ions. 2. The release of transmitter after a nerve impulse is delayed and prolonged in the presence of the four ions, but the amount of evoked transmitter release estimated from the mean quantal content of e.p.p. is increased only by UO22+ and TEA. Both Ni2+ and Zn2+ decrease it. 3. The frequency of m.e.p.p.s is increased by UO22+ and decreased by Ni2+ and Zn2+ at KCl‐depolarized junctions. It is not affected by TEA. 4. It has been concluded that the increased presynaptic spike duration is responsible for the delayed and prolonged transmitter release in the presence of ions which increase the nerve spike duration at Ranvier's node. It is demonstrated that some ‘specific’ effects possibly resulting from ionic competition for presynaptic sites between UO22+, Ni2+ or Zn2+ and other ions present in the Ringer may increase, interfere with, or hide the increased transmitter release that may be predicted from the lengthened presynaptic depolarization.

Presynaptic currents in mouse motor endings

“…The presence of a delayed potassium conductance, g9 at the terminal part is indicated by the action of TEA, 4-AP and 3,4-AP, since the only known property shared by these drugs is their ability to block K channels. The late component of the terminal response is, thus, homologous to the TEA or 4-AP-sensitive deflexion of the triphasic wave former from frog endings (Benoit & Mambrini, 1970) or from experimentally demyelinated internodes of rat nerves (Bostock et al 1981). A restricted area between terminal and preterminal portions shows triphasic (positive-negative-positive) wave forms similar to those obtained in cases of impulse propagation along a linear conductor when the action potential is terminated by a rapid increase in 9K.…”

“…4C1, C2). Benoit & Mambrini (1970) Frankenhauser & Huxley, 1964). Another possibility is that K current is present only at terminal and intermediate portions where it repolarizes rapidly the membrane.…”

“…The negative phase appears composed of two elements whose relative amplitudes varied on small readjustment of electrode position. The segment that generates this wave form lies above the end-plate and does not contact the post-synaptic membrane (Couteaux, 1958) Of the three types of response recorded from mouse motor endings, only the intermediate response resembles the classical triphasic wave form observed in motor terminals of frogs (Katz & Miledi, 1965;Braun & Schmidt, 1966;Benoit & Mambrini, 1970) and rats (Datyner & Gage, 1980) which corresponds to membrane current related to a propagating action potential (Tasaki, 1959;Katz & Miledi, 1965;Bostock et al 1981). The triphasic wave form corresponds thus, successively, to outward passive current, active Na current and delayed outward K current.…”

Barbiturate‐induced transmitter release at a frog neuromuscular junction

“…5). Tetraethylammonium is also thought to increase the release of transmitter at frog end-plates by prolonging the presynaptic action potential (Koketsu, 1958;Benoit & Mambrini, 1970). The possibility that barbiturates affect some additional step in the chain of events leading to transmitter release has not been excluded.…”

The Electrostatic Basis of Mg ++ Inhibition of Transmitter Release

“…side, after entry into the terminal through the calcium channels, acts to increase quantal content; this complicates the interpretation of data obtained with these ions (11,12). On the other hand, Be++ and nonalkali earth multivalent cations (e.g., Mn++, UO2++, Ni++, Zn++, and La+++) undoubtedly can bind to the motor axon and its terminals and thus act at much lower concentrations and in more complicated fashions than Mg++ (12)(13)(14).…”