Abstract
The anterograde transport of horseradish peroxidase (HRP) was utilized to examine the post-lesion expansion of the commissural projection to the molecular layer of the dentate gyrus in adult rats prenatally exposed to ethanol, and in normal and pair-fed controls. Mean daily ethanol consumption by the pregnant dams was 12.0 ± 1.6 g/ kg. Similar consumption in a separate group of pregnant dams produced mean blood ethanol concentrations of 102.8 ± 5.2 mg/ dl of blood. The commissural terminal field of rats exposed to ethanol in utero and given unilateral entorhinal lesions as adults exhibited a significantly greater expansion compared to controls. There were no differences in the HRP-labeled terminal fields between normal and pair-fed animals with similar lesions, suggesting that the effect in the ethanol-exposed rats was due to ethanol teratogenicity rather than reduced caloric intake. Furthermore, the effect was not a function of altered organization of commissural and perforant path terminal fields (terminal field overlap). These data demonstrate that exposure to ethanol in utero produces long-lasting alterations in lesion-induced axon sprouting.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
