Action potentials are electrical impulses which are responsible for relaying a signal along a neuron and play a key role in intra and inter-neuronal communication. They are triggered by influx and outflux of specific ions which initially causes hyperpolarization of the cell membrane. Above a threshold membrane potential an all or nothing cascade of further membrane hyperpolarization occurs which traverses the length of the neuron, this phenomenon is the action potential.

The CNS is comprised of neurons bundled into fibres which may be myelinated or non-myelinated. Myelination of neurons in the CNS occurs via Oligodendrocytes as opposed to Scwann cells in the peripheral nervous system. These oligodendrocytes branch out to ensheath adjacent neuronal axons in insulating myelin which is composed of a high proportion of lipid approximating to 80% of its constituency with the remaining 20% comprised of protein.

An action potential is initialized from the cumulative spikes of postsynaptic membrane potentials in the soma of the neuron. This results from the action of neurotransmitter diffusion from presynaptic neuron across the synaptic cleft and subsequent binding to the specific neurotransmitter receptor on post synaptic neuron dendrites, which in turn stimulates the activation of voltage gated ion channels, allowing sodium ions to diffuse down their concentration gradient into the cell, thus hyperpolarizing the membrane and creating a graded potential which is variable in strength.

In the case of an action potential, if the cumulative graded potentials reach a threshold level at the trigger zone adjacent to the axon hillock, otherwise known as the axon initial segment, which contains the highest density of voltage gated sodium channels (Adachi et al. 2015) then an all or nothing response is achieved and a one-way impulse traverses the entire length of the axon.

The neuron is initially polarized in its resting state at -70mV relative to the extracellular environment. When the summation of multiple ion channel mediated sodium influx results in the membrane potential increasing to a critical threshold level of approximately -55mV, the action potential is propagated. As many more sodium channels are triggered to open, rapidly hyperpolarizing the immediate area of membrane to approximately +40mV. This hyperpolarizing action moves forward to adjacent membrane along the axon. Milliseconds later as the membrane is hyperpolarized, sodium channels close and potassium channels open, which causes outflux of potassium ions which move down the ionic concentration gradient to make the membrane potential even more negative than during rest. This period is the refractory period whereby an action potential cannot occur as membrane is already above the threshold and sodium channels are closed and it also enforces the one-way motion of the action potential. This is the basis for unmyelinated neuron action potentials.

In myelinated neurons, the same channels are involved, the only difference being that the axon filament is coated in a myelin layer produced from adjacent oligodendrocytes which is derivative of cholesterol. This insulates the axon ensuring that the signal is not attenuated through membrane channel leakage as well as reducing charge capacitance of the membrane.

However, narrow junctions or ‘nodes of Ranvier’ occur in series which are exposed membrane gaps in the myelin sheath separating the insulated spans of axon. These nodes contain a high density of voltage gated sodium channels making the membrane more readily polarizable relative to insulated regions, which contain high density of potassium channels and when the signal reaches the node, its embedded sodium channels are activated, allowing for saltatory propagation which boosts the signal whilst simultaneously enhancing the transmission speed of the action potential along the fibre.

In unmyelinated neurons, the signal travels slower and is proportional to the square root of the axon cross sectional diameter. In contrast, impulse speed of myelinated axons is directly proportional to the cross-sectional diameter (Hartline, D.K., Colman, D.R. 2007). Showing that myelination has significant benefits for communication in the central nervous system. Myelination effectively circumvents the requirement for the impulse to jump from ion channel to ion channel as they become activated as is the case with unmyelinated axons. It allows instead for the signal to jump from node to node between insulated regions which is a comparatively  far greater jump and thus allows for greater speeds of transmission.

The physiological implications of myelination can be observed in certain diseases such as multiple sclerosis whereby the myelin sheath undergoes some degree of break down and thus action potentials are diminished and may not traverse the entire length of the axon (Miller, R.H. & Mi, S., 2007). This is due to the lower resistance of the membrane which allows charge to leak out and dissipate.

 

Adachi, R., Yamada, R., Kuba, H., (2015). Plasticity of the axonal trigger zone. The Neuroscientist. 21 (3): 255–265.

Hartline, D.K., Colman, D.R. (2007). Rapid conduction and the evolution of giant axons and myelinated fibers. Current Biology 17(1): R29–R35.

Miller, R.H., Mi, S., (2007). Dissecting demyelination. Nature Neuroscience. 10 (11): 1351–54