Sensitizes adjacent myelinated and unmyelinated nerve fibres

Promotes the rapid death of the cut nerve fibres

Desensitizes adjacent unmyelinated nerve fibres only as myelinated fibres are insulated

Sensitizes adjacent unmyelinated nerve fibres only as myelinated fibres are insulated

Activates the damaged nerves to regrow

Activate different G proteins

Activate different Aα nerve fibres

Activate different TRPV channels

Activate different TRPM8 ion channels

Have different energies to start with

Are all voltage-gated by Na+

Are all chemically-gated by TRPV1

Are a diverse set of channels gated by temperature, pressure and H+.

Are voltage-gated

Are all mechnically-gated

From undamaged myelinated nerve fibres

From the damaged nerve fibres

From the damaged tissue

From damaged myelinated nerve fibres

From undamaged astrocytes and nerve fibres in the area

Opening of TRPM8 and closing of TRPV1 ion channels

Changes in firing rates of warmth fibres and cold fibres

Activation of A-alpha and A-delta nerve fibres in different directions

Activation of A-beta and A-delta nerve fibres

Opening of TRPV1 and closing of TRPM8 ion channels

Primary hyperalgesia is sensitization of bare nerve endings and secondary hyperalgesia is sensitization of encapsulated nerve endings

Primary hyperalgesia is sensitization of the damaged area to non-painful stimuli and secondary hyperalgesia is sensitization of the damaged area to painful stimuli 

Primary hyperalgesia is sensitization of the damaged area and secondary hyperalgesia is sensitization of surrounding skin

Primary hyperalgesia is due to sensitization of TRPV1 channels and secondary hyperalgesia due to sensitization of voltage-gated channels

Primary hyperalgesia is sensitization of the damaged area to painful stimuli and secondary hyperalgesia is sensitization of the damaged area to non-painful stimuli