Subcutaneous injection of formalin produces a biphasic profile of pain
response: a transient early phase followed by a tonic late phase. A n
umber of studies have indicated that the development of the late phase
of formalin pain is dependent upon prolonged changes in central neura
l function produced by neural activity that is generated during the ea
rly phase (i.e. central sensitization). In support of this, the presen
t study demonstrates that stimulation- or morphine-produced analgesia
derived from the periaqueductal grey (FAG) during the early phase prev
ents the development of the late phase. These results suggest that des
cending mechanisms of pain inhibition, as reflected by FAG stimulation
- and morphine-produced analgesia, can prevent the development of cent
ral neural plasticity following injury.