The action of calcium at spinal neurones of the frog

Abstract

SUMMARY1. The action of Ca on membrane excitability and synaptic transmission at motoneurones of the isolated spinal cord of the frog has been studied.2. Impulse propagation along presynaptic fibres was unaffected by [Ca] in the range of 0-10 mm in the presence of 1 mM-Mg. 3. Motoneurone membrane excitability was within normal ranges when the cord was bathed in low or 0 Ca solutions containing 1 mM-Mg but was depressed in 5 or 10 mM-Ca solutions.4. Spontaneous miniature synaptic potentials were recorded in the presence of tetrodotoxin. The frequencies were reduced but not abolished in the absence of bath Ca, but were increased greater than twofold in 5 or 10 mM-Ca in comparison to those in normal Ringer solution (1 mM-Ca).5. Iontophoretic application of Ca both near to and remotely from the intracellular recording site (presumably in the soma) caused facilitation of elicited post-synaptic potentials.6. It is concluded that the action of Ca at these central synapses is identical to that described at the neuromuscular junction.

Effects of some divalent cations on synaptic transmission in frog spinal neurones.

“…For instance, addition of Mg2+ (12-20 mM) to the bathing fluid reduced the amplitude, but did not completely abolish the evoked synaptic potentials (Katz & Miledi, 1963). Similar results were obtained if Ca2+ was removed from the external fluid (Dambach & Erulkar, 1973); although it was later reported (Erulkar, Dambach & Mender, 1974) that transmission was blocked, when bath [Ca2+] was decreased to 0-1 mM and [Mg2+] increased to 5-11 mM.…”

Mechanisms of post‐synaptic excitation in amphibian motoneurones.

“…The spontaneous miniature synaptic potentials which can be recorded from spinal motoneurones in normal Ringer solution could still be seen after suppression of evoked responses by Ca lack and by elevations of the bath Mg2+ as shown previously 440 441 (Katz & Miledi, 1963;Dambach & Erulkar, 1973). In Ringer solution containing 5 mM-Co2+ the frequency of miniature potentials may even be increased after the complete suppression of all chemically mediated synaptic activity, as at the frog neuromuscular junction (Shapovalov, 1962;Weakly, 1973 then the time lag between the onset of the electrically and chemically mediated monosynaptic e.p.s.p.s is 0'5-1*4 msec (0.93 + 0*056 msec, n = 16).…”

“…As at other peripheral and central synaptic junctions with a chemical mode of transmission the effect of Ca2+ on evoked transmitter release occurs also at synapses of frog motoneurones (Katz & Miledi, 1963;Grinnell, 1966;Dambach & Erulkar, 1973;Barrett & Barrett, 1976 The activity of presynaptic fibres from the dorsal root was practically unaffected by reduction in bath Ca2+ or by Mg2+ (5-10 mM) and Mn2+ (2 mM) as evidenced by the amplitude and duration of the presynaptic spike. However, Co2+ (5 mM) or high Mg2+ (20 mM) induced a decrease and prolongation of the presynaptic spike.…”

Separation of two voltage‐sensitive potassium currents, and demonstration of a tetrodotoxin‐resistant calcium current in frog motoneurones.

“…9 were obtained. The twice normal [Ca2+] increased the firing threshold of the neurone from about 22 to 30 mV (depolarization from rest), presumably by altering the voltage dependence of the fast Na+ conductance (see Dambach & Erulkar, 1973;Woodhull, 1973 …”

“…We also made major changes in the bath concentrations of C1-and HCO3-, the only other major univalent ions whose transmembrane equilibrium potentials might normally be negative to the resting potential. These changes included almost total replacement of extracellular Cl-by S042-, intracellular injection of Cl-, and variation of chemical synaptic transmission and the variation of action potential threshold with extracellular [Ca2+] are amply documented (Frankenhaeuser, 1957;Jenkinson, 1957;Katz, 1969;Dambach & Erulkar, 1973;Woodhull, 1973 (Meiri & Rahamimoff, 1972;Kita & van der Kloot, 1973;Weakly, 1973) and Ca2+ influx into axons (Baker et al 1973) and synaptic terminals (Katz & Miledi, 1969a;Blaustein, 1975). Addition of 1-2 mM-Mn2+ or 4-5 mM-Co2+ to the normal Ringer solution perfusing the spinal cord sections abolished the slow afterhyperpolarization within 10-30 min, as illustrated for Mn2+-perfused motoneurones in Figs.…”