Nociception-driven decreased induction of Fos protein in ventral hippocampus field CA1 of the rat.

To test the hypothesis that the hippocampus field CA1 is recruited in nociceptive intensity-dependent fashion in the formalin model of inflammatory pain, we determined the effect of injection of formalin (0.625-2.5%) on the induction of Fos protein along the length of the hippocampus. Compared to injection of saline, injection of formalin (0.625-2.5%) evoked a concentration-dependent increase in nociceptive behavior and a significant linear increase in the number of Fos-positive cells in the spinal cord, especially in the deeper laminae. Injection of saline also increased induction of Fos along the length of hippocampus. On the other hand, injection of formalin decreased the number of Fos-positive cells in whole CA1, CA3 and dentate gyrus, with a greater significant effect in the posterior-ventral regions of the hippocampus. Indeed, a formalin concentration-dependent decrease was observed in the ventral CA1. A systematic pattern of change in Fos induction was not observed in the medial septum region. Of the regions examined, only the formalin-induced changes in Fos cell counts in the posterior and ventral CA1 were tightly correlated with the changes observed in the spinal cord. The foregoing findings suggest that nociceptive information is processed in distributed fashion by the hippocampus, and at least the ventral CA1 is implicated in nociceptive intensity-dependent integrative functions.