Table 1.

Neurochemical signature of inflammatory pain

Experimental models of inflammatory pain
AcuteShort-termLong-term
FORM 8 minFORM 60 minCAR 3 hrCFA 3 dPOLY 21 d
SPR internalization in lamina IYesYesNoNoNo
Synaptic transmissionYesYesYesYesND
Volume transmissionNoNoYesYesND
SPR internalization in lamina I after non-noxious stimulationNDNDYesYesND
SPR internalization in laminae I–III after noxious stimulationNDNDYesYesND
SPR upregulation in lamina INoNoNoYesYes
SPR upregulation on the contralateral sideNoNoNoNoYes
  • In acute inflammatory pain, there is ongoing release of substance P (SP), which induces SPR internalization in lamina I neurons. Although ongoing release of SP is absent in short-term inflammatory pain, SP is released in response to both noxious and non-noxious somatosensory stimulation with a resulting SPR internalization being observed in neurons located in laminae I and III–IV. In long-term inflammatory pain, the same pattern of SP release and SPR activation is observed as with short-term inflammation, but with the addition of a significant upregulation of the SPR in lamina I neurons.