<P> Although action potentials are generated locally on patches of excitable membrane, the resulting currents can trigger action potentials on neighboring stretches of membrane, precipitating a domino - like propagation . In contrast to passive spread of electric potentials (electrotonic potential), action potentials are generated anew along excitable stretches of membrane and propagate without decay . Myelinated sections of axons are not excitable and do not produce action potentials and the signal is propagated passively as electrotonic potential . Regularly spaced unmyelinated patches, called the nodes of Ranvier, generate action potentials to boost the signal . Known as saltatory conduction, this type of signal propagation provides a favorable tradeoff of signal velocity and axon diameter . Depolarization of axon terminals, in general, triggers the release of neurotransmitter into the synaptic cleft . In addition, backpropagating action potentials have been recorded in the dendrites of pyramidal neurons, which are ubiquitous in the neocortex . These are thought to have a role in spike - timing - dependent plasticity . </P> <P> A neuron's ability to generate and propagate an action potential changes during development . How much the membrane potential of a neuron changes as the result of a current impulse is a function of the membrane input resistance . As a cell grows more channels are added to the membrane causing a decrease in input resistance . A mature neuron also undergoes shorter changes in membrane potential in response to synaptic currents . Neurons from a ferret lateral geniculate nucleus have a longer time constant and larger voltage deflection at P0 than they do at P30 . One consequence of the decreasing action potential duration is that the fidelity of the signal can be preserved in response to high frequency stimulation . Immature neurons are more prone to synaptic depression than potentiation after high frequency stimulation . </P> <P> In the early development of many organisms, the action potential is actually initially carried by calcium current rather than sodium current . The opening and closing kinetics of calcium channels during development are slower than those of the voltage - gated sodium channels that will carry the action potential in the mature neurons . The longer opening times for the calcium channels can lead to action potentials that are considerably slower than those of mature neurons . Xenopus neurons initially have action potentials that take 60--90 ms . During development, this time decreases to 1 ms . There are two reasons for this drastic decrease . First, the inward current becomes primarily carried by sodium channels . Second, the delayed rectifier, a potassium channel current, increases to 3.5 times its initial strength . </P> <P> In order for the transition from a calcium - dependent action potential to a sodium - dependent action potential to proceed new channels must be added to the membrane . If Xenopus neurons are grown in an environment with RNA synthesis or protein synthesis inhibitors that transition is prevented . Even the electrical activity of the cell itself may play a role in channel expression . If action potentials in Xenopus myocytes are blocked the typical increase in sodium and potassium current density is prevented or delayed . </P>

Do all neurons have the same action potential