I know that cold receptors have myelinated axons and heat receptors don't.
From a physiological perspective, what could be the consequences if cold receptors were unmyelinated? Would that pose some detrimental effect?
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From a physiological perspective, what could be the consequences if cold receptors were unmyelinated?
Per the resistor-capacitor model of a neuron, one would expect signals conducted through myelinated axons to be faster, more sharply localized in time (spikes don't broaden out as they propagate down the axon), and less costly of energy, vs in unmyelinated axons.
I wouldn't read too much into significance as there's all kinds of ways to accomplish the same effect at any level, e.g. faster conduction is also accomplished through larger axon diameter, and better temporal localization is also accomplished through signal coding, and energy consumption is also modulated by tweaking membrane composition of ion channels etc.
Would that pose some detrimental effect?
Generally, if it's normal for axons to be unmyelinated then one would expect things to be running normally. Demyelination of normally myelinated axons pretty much always leads to loss of function in sensation or motor control.
The question to ask here is rather "Would myelination of normally unmyelinated afferents pose some detrimental effect?" I'm actually not aware of any disorders in which there is "extra myelination" -- Even the dysmyelination disorders are all loss of function in the proteins, not extra insulating myelin or myelination in the wrong place. That doesn't mean there aren't overmyelination disorders, but does suggest that our nervous systems are less sensitive to overmyelination if it is a thing that happens.
One would expect conduction velocity and energy consumption to decrease, okay. Probably not an issue unless temporal synchronization in that signal is important; even then "plasticity" usually irons out these problems.
If the normally unmyelinated afferent axon normally has synapses homogeneously distributed along its shaft, then abnormal myelination could cause abnormal development of these synapses. As contact area would only be available between myelin "nodes," synapses would be crowded into smaller area. Also depending on how development works in the systems you're considering, overmyelination might affect the spatial pattern of secreted growth factor concentration which could affect synaptic development along the axon shaft. But this is all completely hypothetical.