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Effects of calcium and magnesium on transmitter release at Ia synapses of rat spinal motoneurones in vitro.

The lumbar spinal cord excised from neonatal rats was superfused with an oxygenated saline, and monosynaptic excitatory post‐synaptic potentials (e.p.s.p.s) were recorded from the lumbar motoneurones following stimulation of muscle nerves of the hind leg. The amplitude of monosynaptic e.p.s.p.s increased with an increase in the external Ca2+ concentration ([Ca2+]o). In [Ca2+]o of 0.5‐2 mM, the relation between the e.p.s.p. amplitude and [Ca2+]o was linear with a slope of 1.6 on double logarithmic co‐ordinates. An increase in [Mg2+]o in a range of 1‐5 mM reduced the e.p.s.p. amplitude without affecting the slope of the relation between log e.p.s.p. amplitude and log [Ca2+]o, suggesting competitive interaction between Ca2+ and Mg2+. When [Ca2+]o was increased to 4‐12 mM, the latency of monosynaptic e.p.s.p.s was prolonged, and the antidromic action potential failed to invade the cell body or initial segment of motoneurones. Under these conditions, the monosynaptic e.p.s.p.s were still present. It is concluded that at near‐normal levels of [Ca2+]o the effects of Ca2+ and Mg2+ on the e.p.s.p. amplitude are accounted for entirely by their competitive interaction for the probability of transmitter release without altering the mode of impulse propagation at central terminals of the Group Ia sensory fibres. It is suggested that impulses of Ia sensory fibres normally invade their terminals without intermittent blocks at their terminal branch points.