A solution to the problem of morphine tolerance and associated nerve damage.

Joyce DeLeo of Dartmouth Medical School wondered about immune cell involvement in tolerance to morphine. Hear how she explored the subject and her fascinating findings. This short summary of her work has a few difficult words for laypeople which I have explained in notes at the bottom of this entry.

From:
http://www.the-scientist.com/2005/03/28/S26/1

"After studying the role of microglia (*) in neuropathic pain for many years, DeLeo applied similar experimental strategies to study the hyperalgesia observed in morphine-dependent animals and its interactions with nerve injury.

"First, she showed the decreased effect that morphine has on pain behaviors in her nerve injury model; this imitates the clinical problem with opiate resistance in neuropathic pain patients.

"Second, she found that chronic morphine treatment activated spinal microglia and concomitantly increased proinflammatory cytokines. These changes were amplified in animals with nerve injury. Given the likelihood that activated microglia enhance pain sensation, it follows that morphine administration is actually exacerbating the effect.

"By giving cytokine inhibitors (*), DeLeo was able to restore morphine's effectiveness.

Note: Microglia: A type of immune cell found in the brain. Microglia are scavengers, engulfing dead cells and other debris. In Alzheimer’s disease, microglia are found associated with dying nerve cells and amyloid plaques.

Note: Cytokine inhibitors: cytokines are cells that facilitate communication among immune system cells. Obviously, then cytokine inhibitors are substances that stop the immune system communicating well.