Alcohol-, nicotine-, and cocaine-evoked release of morphine from human white blood cells: substances of abuse actions converge on endogenous morphine release.

BACKGROUND

Normal human white blood cells (WBC) have the ability to synthesize morphine as do invertebrate ganglia. Furthermore, invertebrate neural tissues incubated with ethanol, cocaine, or nicotine results in a statistically significant enhancement of labeled morphine release. We now demonstrate that this also occurs with human WBC.

MATERIAL/

METHODS

Human blood was obtained from the Long Island Blood Services (Melville, NY). Polymorphonuclear cells (PMN) or mononuclear cells (MN) (10 million/ml) were bathed in phosphate buffered saline (PBS) medium containing purified RIA grade 125I-labeled morphine for trace labeling and quantification of media concentrations of morphine were via RIA. Cells were then incubated with cocaine, alcohol or nicotine and morphine release was determined. Residual levels of radioactivity in control tissues were always greater than 65% of total cpm, whereas in treated tissue differences depended on the amount of drug added.

RESULTS

Incorporation rates of 125I-labeled morphine into PMN and MN were 7.85+/-0.36% and 1.42+/-0.19%, respectively. Separate incubations of PMN with ethanol, cocaine, or nicotine resulted in a statistically significant enhancement of 125I-labeled morphine released into the extracellular medium in a concentration dependent manner.

CONCLUSIONS

These substances of abuse have been linked into a common pathway because of the common dopamine connection. Now, they are additionally linked because of their common effect on endogenous morphinergic processes. It is highly significant that these substances of abuse converge on a similar process, providing a mechanism to initiate their pleasure and addicting actions with continued frequent use.