Fibre types

Sensory nerves

Sensory fibre types are often confused because the same fibres are often placed into two different groups (depending on if they are cutaneous or deep/muscle afferents).  In principle:

  • Muscle afferents (e.g. in the muscle spindle) are classed according to their fibre diameters and are typed I, II, III and IV (I being the thickest)
  • Cutaneous afferents (e.g. in the skin) are classified according to their conduction speed and are typed Aα, Aβ, Aδ and C (Aα being the fastest).
    • NB C fibres (IV fibres) are unmyelinated.  The rest are myelinated (various degrees).

In any one peripheral nerve, there are relatively equal amounts of each fibre.  The result (compound action potential- the sum of all the action potentials in one nerve) is a relative spread of signal based on the different speeds of conduction between the different fibre types.

NOTE this is NOT a picture of an action potential, but the change in potential along theentire nervewith time.  From this, you can see that Aα/β fibres are quickest whereas C fibres are slow.  The reason for this, however, is mainly due to the response of different fibres to stimuli, NOT the speed of the AP (the difference between the difference A fibres may be due, at least in part, to AP speed, but this is not the case between A and C fibres).

In general, most non-nociceptive afferents are Aβ fibres (e.g. pacinian / meissner’s / merkels / ruffini).  Nociceptive afferents are mostly C and Aδ fibres.

Out of the nociceptive neurons, Aδ fibres only respond to mechanical and thermal stimuli, whereas C fibres respond to these AND chemical/pH stimuli (and thus local inflammation produced after initial stimulus).

NB The significance of the two temperatures seem to be that 43°C is where warmth becomes burning heat and 53°C is when tissue damage occurs.

Nociceptive fibres have multiple functions

The primary function of nociceptive fibres is to signal to the brain.  It does this via glutaminergic transmission (fast) at the spinal cord.  However, the transmission of ‘pain’ signals from nociceptive neurons is mediated also by their release of peptide molecules in the dorsal horn (mainly tachykinins e.g substance P, neurokinin A) which induce a local inflammation at the DRG and act on interneurons to increase the sensitivity of signal transmission.

This can result in hyperalgesia (a heightened response to noxious stimuli) and/or allodynia (noxious response to non-noxious stimuli).

As well as their afferent function, nociceptive neurons have efferent function in releasing neurogenic inflammatory mediators (e.g. substance P, Calcitonin gene-related protein (CGRP)) at the site of stimulation via signal transmission between branched nerve endings to induce a local neurogenic inflammation that can act in a similar way as above but also activate C fibres in the longer term.


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