Development under the influence of cocaine. II. Comparison of the effects of maternal cocaine and associated undernutrition on brain myelin development in the offspring.

Pregnant and lactating Long-Evans rats were treated daily with oral cocaine at a dosage rate of 60 mg/kg/day, which is the highest dosage tolerated during chronic treatment. Brain myelin concentrations were compared in the offspring during early myelination (day 15) and peak myelination (day 20). Body and brain weights in the offspring of cocaine-treated and pair-fed dams were transiently (but insignificantly) retarded, and by day 20 brain weights of the normal controls, cocaine-exposed, and pair-fed pups were the same (1.36 +/- 0.01-1.35 +/- 0.01 g). Similarly, specific myelin yields in the offspring of pair-fed dams were retarded by no more than 1-2% of the myelin concentrations obtained in normal controls, which is consistent with studies showing that such minimal growth retardation would not be expected to produce hypomyelination. In contrast, myelin concentrations from the brains of cocaine-exposed pups were reduced about 10%. In addition, cross-fostering indicated that the fetal period of cocaine exposure presents a greater risk to postnatal myelination than exposure during the suckling period, which is the reverse of the vulnerability resultant from undernourishment. Thus, the hypomyelination observed in the offspring of cocaine-treated dams indicates a toxic effect of cocaine acting directly on the developing offspring.