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Morphine Harms Brain Cells in Human Fetuses

DNA fragmentation in fetal microglia and neurons increased with higher morphine levels and longer exposure.

Alcohol produces neuronal degeneration in rat fetuses via apoptosis (i.e., programmed cell death) (see Journal Watch Psychiatry Apr 1 2000). In this study, researchers examined the effect of morphine on apoptosis in human neuron, microglia, and astrocyte cultures that were prepared from 16- to 22-week-old aborted fetuses. Investigators grew the cultures in media with or without morphine at various concentrations and assessed apoptosis by measuring DNA fragmentation. Some cultures were pretreated with the narcotic antagonist naloxone or with a caspase inhibitor (increased levels of caspase, a protease, are observed in apoptosis).

Compared with nonexposure, exposure to morphine was significantly associated with higher amounts of DNA fragmentation in microglia and in neurons; DNA fragmentation increased with higher morphine levels and longer exposure. Morphine-exposed astrocytes were spared from apoptosis. Treatment with the caspase inhibitor or naloxone significantly reduced the apoptotic effects of morphine in neurons and in microglia.

Comment: These results, coupled with results from research on alcohol and cocaine (see Journal Watch Psychiatry May 23 2000), strongly suggest that the fetuses of women who use alcohol or morphine during pregnancy are at increased risk for increased brain-cell death. These accumulating findings may make legislation that criminalizes the behavior of pregnant addicts seem not so unreasonable.

— Barbara Geller, MD

Published in Journal Watch Psychiatry September 4, 2002

Citation(s):

Hu S et al. Morphine induces apoptosis of human microglia and neurons. Neuropharmacology 2002 May; 42:829-36.

• Medline abstract (Free)