Abstract
Maintenance with methadone is standard treatment for opioid-addicted patients, including pregnant women. Cellular effects of methadone exposure during development are investigated by using an avian model, which is free of confounding maternal variables. In the first study, which explored dose by duration interactions, methadone was administered at one of two doses (0.458 mg/kg or 1.75 mg/kg) for one of three durations of exposure: late in development (Incubation Days 12 to 19), middle to late (Days 9 to 19), or early to late (Days 5 to 19). In the second study, 1.00 mg/kg of methadone was administered from days 8 to 18 and compared with controls (0.00 mg/kg). Brain tissue and blood samples were harvested for all dose conditions from the two studies. Increased methadone exposure was associated with subependymal anomalies, subependymal hemorrhaging, edema, monocytic infiltration, an increase in disintegrating red blood cells, an increase in white blood cells, and a decrease in neurons. Significant differences in variance for cell counts by condition were observed. Exposed specimens had significantly more thrombocytes (t = - 2.66, p < 0.05). The anomalies suggest that methadone exposure may be harmful to develop organisms at the cellular level.
Highlights
Maintenance therapy with methadone is standard practice for treating pregnant heroin users
The analgesic properties of methadone are due to its structural similarity to endogenous enkephalins and endorphins
This study, through an examination of blood cells and brain tissues from chicks exposed in ova during development, suggests that methadone directly causes changes at the cellular level, changes which cannot be attributed to maternal factors
Summary
Maintenance therapy with methadone is standard practice for treating pregnant heroin users. Maintenance improves psychosocial circumstances for mothers and increases medical compliance among pregnant patients [1]; but, many at-risk women abuse medical opioids during pregnancy [2]. Methadone is a pure mu-opioid agonist without significant kappa or delta receptor activity [8]. It has an affinity for the N-methyl-D-aspartate (NMDA) inotropic glutamate receptors where endogenous enkephalins and beta endorphins bind. Mu-opioid receptors mediate changes in neural transmission by way of inhibition of presynaptic release of GABA [9]. Like other drugs of abuse, opioids lead to release of dopamine in the nucleus accumbens
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