Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats.
Level 5 - mechanism / opinion, no new human data
Preclinical animal study measuring dopamine release in rats.
PubMed 2899326 · doi:10.1073/pnas.85.14.5274
What was done
Brain microdialysis was performed in freely moving rats to measure extracellular dopamine concentrations in two brain regions: the nucleus accumbens septi (mesolimbic) and the dorsal caudate nucleus (motor). The investigators tested drugs abused by humans (opiates, ethanol, nicotine, amphetamine, cocaine), aversive substances (kappa opioid agonists U-50,488, tifluadom, bremazocine), haloperidol, and non-abused drugs (imipramine, atropine, diphenhydramine). Behavioral motility was also observed.
What was found
The abstract reports no numerical values, concentrations, or statistical parameters. Directionally, drugs abused by humans increased extracellular dopamine in both areas, preferentially in the nucleus accumbens, and elicited hypermotility at low doses. Aversive kappa agonists decreased dopamine release in both areas and caused hypomotility. Haloperidol increased dopamine concentrations without preferential accumbens selectivity and caused sedation/hypomotility. Non-abused drugs failed to alter synaptic dopamine levels.
Why it matters
This study provided foundational experimental evidence linking the reinforcing actions of diverse drugs of abuse to preferential dopamine elevation within the mesolimbic system.
Limits
The study was conducted entirely in rodents and does not establish human neurochemical responses directly. The abstract omits sample sizes (n), baseline concentrations, specific dosages, magnitude of dopamine changes, and statistical significance values.
Cited by
- supports Almost every drug of addiction, including nicotine, alcohol, heroin, cocaine, and amphetamine, hijacks the brain's dopamine system.