This work was supported by U.S. Public Health Service Grants AA06916, AA007568, and DE07734.
Migration of Cortical Neurons Is Altered by Gestational Exposure to Ethanol
Version of Record online: 11 APR 2006
Alcoholism: Clinical and Experimental Research
Volume 17, Issue 2, pages 304–314, April 1993
How to Cite
Miller, M. W. (1993), Migration of Cortical Neurons Is Altered by Gestational Exposure to Ethanol. Alcoholism: Clinical and Experimental Research, 17: 304–314. doi: 10.1111/j.1530-0277.1993.tb00768.x
- Issue online: 11 APR 2006
- Version of Record online: 11 APR 2006
- Received for publication June 9, 1992; accepted August 28, 1992
- Cerebral Cortex;
- Fetal Alcohol Syndrome
Rats prenatally exposed to ethanol exhibit a variety of structural anomalies in the central nervous system. One of the key features of experimental fetal alcohol syndrome is microencephaly. Cerebral cortex is particularly susceptible to the effects of prenatal exposure to ethanol. Its total mass is reduced, it is thinner, and it contains fewer neurons and glia. Various studies in rats and humans suggest that chronic early exposure to ethanol leads to a massive reorganization of cortex characterized by heterotopic clusters of neurons. A pulse and chase study with [3H]thymldine autoradiography was used to determine if gestational exposure to ethanol leads to defects in neuronal migration. Rats were fed an ethanol-containing diet between gestational day (G) 6 and G21, pair-fed a liquid control diet, or fed chow. Ethanol delayed the migration of early-generated neurons (those born on G13) to deep cortex by 2 days. Moreover, the migration of late-generated neurons (those born on G21) was delayed 4 to 6 days by ethanol, and often these neurons terminated their migration in ectopic locations. Ethanol significantly decreased the rate of migration and the time postmitotic cells remained in the proliferative zones. On the other hand, ethanol did not have a significant effect on the rate of cortical expansion and the fraction of cells that left the proliferating population in order to migrate to cortex. Thus, the migration of young neurons was profoundly altered by prenatal exposure to ethanol. Such delays may lead to a desynchronization of cortical development that makes it impossible for cortical neurons to establish a normal circuitry.