Vol. 6, No. 2, 2000 Page 7
Vol. 6, No. 2, 2000 Page 7 |
Babies whose mothers drink during pregnancy are at high risk for fetal alcohol syndrome (FAS), a leading cause of mental retardation. Recent reports (see Crime Times Vol. 6, No. 1, page 7) (see related article, Crime Times, 2000, Vol. 6, No. 1, Page 7) indicate that a large percentage of incarcerated offenders suffer from either FAS or fetal alcohol effects (FAE), a milder form of FAS.
A new study indicates that the damage that leads to FAS or FAE stems from alcohol’s effects on receptors for two neurotransmitters, glutamate and GABA. Chrysanthy Ikonomidou et al. report that rats experiencing a single exposure to high blood alcohol duri ing the first two weeks after birth (a time when rats experience stages of brain development similar to those late in human fetal development) experience a “massive wave of cell suicide,” which the researchers have linked to the excessive activation of GA ABA receptors and the blocking of N-methyl-D-aspartate (NMDA) receptors for glutamate.
Eventually, experts say, these findings could translate into treatments that could lessen the damage caused by prenatal exposure to alcohol. For now, according to neurobiologist David Lovinger, who reviewed the study, the most important conclusion to be d drawn from the research is that late-pregnancy drinking “is really unsafe for the brain.”
In an earlier study on young rats, the same researchers found that certain drugs of abuse-including PCP (“angel dust”), ketamine (“special K”), and nitrous oxide (“laughing gas”)-caused massive cell death, also by interfering with NMDA receptors. Normally y, cells are extensively “pruned” during early development. However, Ikonomidou says, “These drugs don’t just cause cells that are going to die anyway to die more quickly. They cause cells that never would have died under normal circumstances to commit su uicide, and millions of cells are involved.”
“Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome,” Chrysanthy Ikonomidou, Petra Bittigau, Masahiko J. Ishimaru, David F. Wozniak, Christian Koch, Kerstin Genz, Madelon T. Price, Vanya Stefovska, Friederike Hörster, Tanya Tenkova, K Krikor Dikranian, and John W. Olney, Science, Vol. 287, February 11, 2000, pp. 1056-1060. See also: “Blockage of NMDA receptors and apoptotic neurodegeneration in the developing brain,” Chrysanthy Ikonomidou et al., Science, Vol. 283, No. 53 398, January 1, 1999, pp. 70-74. Address: Chrysanthy Ikonomidou, Dept. of Pediatric Neurology, Charite-Virchow Clinics, Humboldt University, Augustenburger Platz 1, 13353 Berlin, Germany.