INHIBITION OF NOXIOUS STIMULUS-EVOKED PAIN BEHAVIORS AND NEURONAL FOS-LIKE IMMUNOREACTIVITY IN THE SPINAL-CORD OF THE RAT BY SUPRASPINAL MORPHINE

In previous studies, we reported that supraspinally administered DAMGO , a mu-opioid agonist, produces a dose-related, naloxone-reversible in hibition of formalin-evoked pain behaviors and spinal cord Fos-like im munoreactivity (FLI) in the rat spinal cord. Although these results su pport the hypothesis that activation of supraspinal mu-opioid receptor s produces antinociception by increasing the activity of bulbospinal i nhibitory pathways, other studies suggest that supraspinal morphine de creases rather than increases descending inhibitory control. In the pr esent study, we specifically examined the effect of intracerebroventri cular (i.c.v.) injection of morphine in the rat. Supraspinal morphine produced a dose-related, naloxone-reversible inhibition of both formal in-evoked behaviors and spinal cord FLI. Although the magnitude of the antinociception produced by i.c.v. morphine in the formalin test was significantly correlated with the numbers of FLI neurons in the spinal cord, the lowest dose of i.c.v. morphine tested (0.70 nmol) produced a significant reduction of FLI in the superficial laminae without prod ucing behavioral antinociception, which is consistent with our hypothe sis that noxious stimulus-evoked Fos expression in the superficial lam inae is a poor predictor of the magnitude of pain behavior. These data support the hypothesis that the antinociceptive effects of supraspina lly administered morphine result from an increase in descending inhibi tory control.