An opioid binding protein is specifically down-regulated by chronic morphine treatment in dorsal root and trigeminal ganglia.

Abstract

Despite the recent cloning of mu, delta and kappa opioid receptors, a role in opioid receptor function for an opioid binding cell adhesion molecule is supported by several lines of evidence, including inhibition of opioid binding by opioid binding cell adhesion molecule antibodies, down-regulation of opioid binding cell adhesion molecule by chronic opioid agonist treatment of cultured NG108-15 cells, and reduction of opioid binding in NG108-15 cells by transfection of opioid binding cell adhesion molecule antisense cDNA. In the present study, we report that chronic in vivo treatment of mice with morphine results in down-regulation of opioid binding cell adhesion molecule immunoreactivity in primary afferent neurons in dorsal root and trigeminal ganglia as well as their axons. This effect was blocked by the opioid antagonist naloxone. Down-regulation of opioid binding cell adhesion molecule immunoreactivity was not observed in other areas of the central nervous system. Taken together, the previous studies which demonstrated the role played by opioid receptors in regulating release of transmitters from primary afferent neurons and the present findings of a specific regulation of opioid binding cell adhesion molecule expression by chronic exposure to morphine, provides evidence from an in vivo perspective which advances the notion that opioid binding cell adhesion molecule plays a role in the action of opioids.