Activation of mesocorticolimbic reward circuits for assessment of relief of ongoing pain: a potential biomarker of efficacy.
Level 5 - mechanism / opinion, no new human data
Preclinical animal study measuring neurochemical and behavioral endpoints.
PubMed 24861580 · doi:10.1016/j.pain.2014.05.018
What was done
Researchers evaluated extracellular dopamine release in the nucleus accumbens shell via microdialysis in awake rats subjected to either post-surgical incisional pain (1 day post-incision) or neuropathic pain (14 days post-spinal nerve ligation [SNL]). They tested whether analgesics with distinct clinical indications (spinal clonidine, gabapentin, ketorolac, and naproxen) produced conditioned place preference and selective mesolimbic dopamine efflux in pain-matched models compared with sham-operated controls.
What was found
The abstract reports no numerical values or effect sizes. Basal dopamine levels did not differ across groups, and no treatment effects were observed in sham-operated animals. Spinal clonidine produced conditioned place preference and a dose-related increase in nucleus accumbens dopamine release in SNL rats. Gabapentin increased nucleus accumbens dopamine in SNL rats but not in rats with incisional injury. Conversely, ketorolac and naproxen increased dopamine release in rats with incisional pain but not in those with neuropathic pain.
Why it matters
Nucleus accumbens dopamine efflux in preclinical models may provide an objective neurochemical biomarker of pain relief to assess novel analgesic mechanisms.
Limits
The abstract does not report sample sizes, specific dosages, or numerical dopamine concentrations. As an animal model study, findings in rodents may not directly translate to human clinical pain conditions.
Cited by
- supports The cessation or removal of a painful or difficult stimulus causes a neurochemical increase in catecholamines including dopamine, epinephrine, and norepinephrine.