Table 1.

Neurochemical signature of inflammatory pain

	Experimental models of inflammatory pain
	Acute		Short-term	Long-term
	FORM 8 min	FORM 60 min	CAR 3 hr	CFA 3 d	POLY 21 d
SPR internalization in lamina I	Yes	Yes	No	No	No
Synaptic transmission	Yes	Yes	Yes	Yes	ND
Volume transmission	No	No	Yes	Yes	ND
SPR internalization in lamina I after non-noxious stimulation	ND	ND	Yes	Yes	ND
SPR internalization in laminae I–III after noxious stimulation	ND	ND	Yes	Yes	ND
SPR upregulation in lamina I	No	No	No	Yes	Yes
SPR upregulation on the contralateral side	No	No	No	No	Yes

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.