Cocaine-induced somatic growth deficit during the brain growth spurt is prevented by artificial-rearing.
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abstract
The brain growth spurt is a dynamic period of central nervous system development that has been shown to be particularly vulnerable to a variety of insults. This study was designed to assess the effects of various doses of cocaine during this potentially vulnerable period on survival rate, somatic growth, and brain development, utilizing an artificial-rearing paradigm. Three cocaine-treated groups received SC administration of either 40, 60, or 80 mg/kg/day of cocaine HCl from postnatal days 4 through 9. There were significant differences in survival rates among 60 and 80 mg/kg/day cocaine-treated animals as compared with gastrostomy controls. No statistically significant differences were found with regard to body and brain weights between the various cocaine-treated groups and the gastrostomy control group. Additionally, there was no evidence of cocaine's effect on forebrain, cerebellum, or brainstem weights when compared with individually corresponding controls. Taken together with our previous results, these data suggest that cocaine administration during the brain growth spurt period produces a dose-related increase in lethality, and the use of artificial-rearing method seems to lower the lethal threshold of cocaine among these neonates. However, no statistically significant effects of cocaine exposure on brain weight measures were obtained. The most important finding was that the cocaine-induced somatic growth retardation observed previously under normal-rearing conditions was eliminated by using a nutritionally controlled artificial-rearing paradigm, suggesting that cocaine-induced restriction of somatic growth may be a function of interference with normal feeding behavior, and therefore, a secondary effect of cocaine exposure during development.
