Author(s): Leskawa KC, Jackson GH, Moody CA, Spear LP
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Abstract Behavioral dysfunctions in offspring exposed in utero to cocaine have been observed, along with alterations in dopamine systems, but few studies of the underlying biochemistry have been conducted. Because of their documented roles in neuronal maturation, glycosphingolipids were analyzed in whole brains of offspring exposed gestationally to cocaine. Rat offspring exposed to cocaine in utero exhibited markedly elevated levels of both total gangliosides (p < 0.001) and neutral glycosphingolipids (p < 0.01) at postnatal day 1. However, by postnatal day 11 levels of gangliosides and neutral glycosphingolipids returned to control values. These effects were not restricted to chronic cocaine exposure early in life, in that ganglioside content of whole maternal brains was also elevated (p < 0.001), though less than that observed with the neonate brains. Qualitatively, no differences in ganglioside nor neutral glycolipid structure distribution were observed between cocaine-exposed and normal animals following separation by HPTLC and HPLC. These elevations are in contrast to those following alcohol exposure, where decreases in brain gangliosides have been observed. Neurochemical consequences of prenatal exposure to cocaine may be far-reaching and may not be restricted to the dopamine system.
This article was published in Brain Res Bull
and referenced in Journal of Biomolecular Research & Therapeutics