Abstract
Repetitive firing (RF) as two or more end plate currents (EPC) induced by a single stimulus of the motor nerve was studied in sartorius frog muscle under voltage clamp conditions. In the presence of 4-aminopyridine (1.10−4 M), RF as two EPC with 3–8 msec intervals was found in half of the cells (n=35). When calcium ion concentration was increased from 1.8 to 5.4 mM, magnesium to 5–9 mM, and rhythmic activity beginning with 0.05 Hz and above, RF stopped, but when strontium or barium was substituted for calcium, RF intensified. In the presence of barium, the repeated EPC quantity reached six-eight per one nerve impulse. Slow currents arose in some of the cells when disruption of the EPC series was stimulated. Proserine, an anticholinesterase agent, enhanced RF, whereas α-bungarotoxin, a cholinoreceptor blocker, had no effect. The role that calcium and calcium-activated potassium currents play in generating and terminating mechanisms of RF, is discussed.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
Literature cited
A. L. Zefirov and I. A. Khalilov, "Properties of electrical activities in different parts of the frog nerve ending," Byull. Éksp. Biol. Med.,94, No. 1, 7–10 (1985).
P. G. Kostyuk, Calcium and Cell Excitability [in Russian], Nauka, Moscow (1986), p. 255.
L. G. Magazanik, E. E. Nikol'skii, and R. A. Giniatullin, "Dependence of end plate current decay rate on size of the quanta composition and previous synaptic activity," Dokl. Akad. Nauk,271, No. 2, 489–492 (1983).
B. I. Khodorov, General Physiology of Excitable Tissues [in Russian], Nauka, Moscow (1975), p. 406.
E. Aizenman, G. G. Bierkamper, and E. F. Stanley, "Botulinum toxin prevents stimulusinduced backfiring produced by neostigmine in the mouse phrenic nerve diaphragm," J. Physiol.,372, 395–404 (1986).
A. J. Anderson and A. L. Horvey, "ω-Conotoxin does not block the verapamil-sensitive calcium channels at mouse nerve terminals," Neurosci. Lett.,82, No. 1, 117–180 (1987).
G. J. Augustine and R. Eckert, "Divalent cations differentially support transmitter release at the squid giant synapse," J. Physiol.,346, 257–271 (1984).
W. M. Fu, R. H. Lin, and S. Y. Lin-Shian, "Study on the neuromuscular action of 4-aminopyridine in the mouse diaphragm," Arch. Int. Pharmacodyn. Ther.,289, No. 2, 198–211 (1987).
M. I. Glavinovic, "Differences in presynaptic action of 4-aminopyridine and tetraethylammonium at the frog neuromuscular junction," Can. J. Physiol. Pharmacol.,65, No. 3, 747–752 (1987).
A. L. Gorman and A. Hermann, "Internal effects of divalent cations on potassium perability in molluscan neurons," J. Physiol.,296, February, 393–410 (1979).
A. Hermann and A. L. Gorman, "The calcium dependence of the slow inward currents in theAplysia pacemaker cell R-15," Pflugers. Arch.,382, Suppl., 38 (1979).
E. Hevron, G. David, A. Arnon, and Y. Yaari, "Acetylcholine modulates two types of presynaptic potassium channels in vertebrate motor nerve terminals," Neurosci. Lett.,72, No. 1, 87–92 (1986).
R. Hohfeld, R. Sterz, and K. Peper, "Prejunctional effects of acetylcholinesterase drugs at the endplate mediated by presynaptic acetylcholine receptors or by postsynaptic potassium efflux," Pflugers Arch.,391, No. 1, 213–218 (1981).
P. Illes and S. Thesleff, "4-Aminopyridine and evoked transmitter release from motor nerve endings," Br. J. Pharmacol.,64, No. 4, 623–629 (1978).
B. Katz and R. Miledi, "The role of calcium in neuromuscular facilitation," J. Physiol.,195, No. 2, 481–492 (1968).
B. Katz and R. Miledi, "Spontaneous and evoked activity of motor nerve endings in calcium Ringer," ibid.,203, No. 3, 689–706 (1969).
P. G. Kostyuk, P. A. Dorochenko, and A. E. Martynyuk, "Fast decrease of the peak current carried by barium ions through calcium channels in the somatic membrane of mollusc neurons," Pflugers Arch.,404, No. 1, 88–90 (1985).
H. Lundh, "Effects of 4-aminopyridine on neuromuscular transmission," Brain Res.,153, No. 2, 307–318 (1978).
A. Mallart, "Presynaptic currents in frog motor nerve endings," Pflugers Arch.,400, No. 1, 8–13 (1984).
A. Mallart, "A calcium-activated potassium current in motor nerve terminals of the mouse," J. Physiol.,368, February, 577–591 (1985).
I. G. Marshall, J. J. Lambert, and N. N. Durant, "Inhibition of aminopyridine-induced contractile activity in skeletal muscle by tetrodoxin and by magnesium," Eur. J. Pharmacol.,54, No. 1, 9–14 (1979).
M. D. Miyamoto, "The action of cholinergic drugs on motor nerve terminals," Pharmacol. Rev.,29, No. 3, 221–247 (1977).
J. M. Molgo, M. Lemeignan, and P. Lechat, "Effects of 4-aminopyridine at the frog neuromuscular junction," J. Pharmacol. Exp. Therap.,250, No. 1, 121–142 (1975).
J. Molgo and S. Thesleff, "Electrotonic properties of motor nerve terminals," Acta Physiol. Scand.,114, No. 2, 271–275 (1982).
W. H. Moolenaar and I. Spector, "The calcium action potential and a prolonged calcium dependent after-hyperpolarization in the mouse neuroblastoma cells," J. Physiol.,292, May, 297–306 (1979).
L. D. Pertidge, "A mechanism for the control of low-frequency repetitive firing," Cell Mol. Neurobiol.,2, No. 1, 33–45 (1982).
R. Penner and F. Dreyer, "Two different presynaptic calcium currents in mouse motor nerve terminals," Pflügers Arch.,406, No. 2, 190–197 (1986).
M. A. Rogawski and J. L. Barker, "Effects of 4-aminopyridine on calcium action potentials and calcium current under voltage clamp in spinal neurons," Brain Res.,280, No. 1, 180–185 (1983).
Additional information
S. V. Kurashov Medical Institute, Russian Federation Ministry of Public Health, Kazan. Translated from Neirofiziologiya, Vol. 24, No. 4, pp. 387–395, July–August, 1992.
Rights and permissions
About this article
Cite this article
Giniatullin, R.A. Repetitive firing in motor nerve endings: Divalent cation, rhythmic activity, and cholinergic agent modulation. Neurophysiology 24, 237–243 (1992). https://doi.org/10.1007/BF01057324
Received:
Issue Date:
DOI: https://doi.org/10.1007/BF01057324