Abstract
Myelin is the multi-layered lipid sheet periodically wrapped around neuronal axons. It is most frequently found in vertebrates. Myelin allows for saltatory action potential (AP) conduction along axons. During this form of conduction, the AP travels passively along the myelin-covered part of the axon, and is recharged at the intermittent nodes of Ranvier. Thus, myelin can reduce the energy load needed and/or increase the speed of AP conduction. Myelin first evolved during the Ordovician period. We hypothesize that myelin's first role was mainly energy conservation. During the later “Mesozoic marine revolution,” marine ecosystems changed toward an increase in marine predation pressure. We hypothesize that the main purpose of myelin changed from energy conservation to conduction speed increase during this Mesozoic marine revolution. To test this hypothesis, we optimized models of myelinated axons for a combination of AP conduction velocity and energy efficiency. We demonstrate that there is a trade-off between these objectives. We then compared the simulation results to empirical data and conclude that while the data are consistent with the theory, additional measurements are necessary for a complete evaluation of the proposed hypothesis.
Highlights
Myelin is a neural cellular specialization unique to vertebrates
THE HYPOTHESIS Our hypothesis is that during the Mesozoic marine revolution, the role of myelin changed from mainly improving the energy efficiency of action potentials (APs) conduction to improving conduction speed
If the Mesozoic marine revolution and the subsequent increase in marine predation pressure did not cause a change in the role of myelin, the parameters of myelinated axons should be relatively uniform in all vertebrate lineages
Summary
Myelin is a neural cellular specialization unique to vertebrates (with a few interesting exceptions, Davis et al, 1999; Hartline and Colman, 2007). The more actively moving animals, which came to dominate ecosystems, used myelin for increasing the propagation speed of neural signals (Figure 2) This should true for predators as well as for the prey in need of improved escape behavior. If the Mesozoic marine revolution and the subsequent increase in marine predation pressure did not cause a change in the role of myelin, the parameters of myelinated axons should be relatively uniform in all vertebrate lineages. To reformulate our hypothesis in this framework, we believe that the set-point of the evolutionary optimization process shifted on the continuum toward transmission speed during the Mesozoic marine revolution, and it shifted to different new set-points in different vertebrate lineages. We discuss future experimental work to further test our hypothesis, as well as the implications of our hypothesis for medical research
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