Abstract
We examined the effects of 4-aminopyridine (4-AP) on calcium conductance mechanisms in cultured mouse spinal cord neurons. At low concentrations (⩽ 1mM), 4-AP enhanced Ca 2+-dependent transmitter release and prolonged the duration of Ca 2+-dependent action potentials. Voltage clamp studies indicated that 4-AP directly facilitates Ca 2+ entry through voltage sensitive channels apart from an effect on K + currents. These results may help to explain why the drug promotes Ca 2+-dependent transmitter release at peripheral and central synapses.
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