Abstract:
:This work explores the hypothesis that perturbations caused by ethanol on the regulatory role of retinoids in brain development may be a mechanism involved in the neuropathology of fetal alcohol syndrome. The interaction of ethanol and retinoic acid (RA) on RA receptor (RAR) beta and glial fibrillary acidic protein (GFAP) mRNA expression is evaluated. In the U-373 MG astrocytoma, mRNA expression of RAR beta was increased and GFAP was decreased by RA. Ethanol decreased the expression of RAR beta mRNA, but increased that of GFAP. The RA-stimulated increase in RAR beta was not affected by the presence of ethanol. RA prevented the ethanol-induced increase in GFAP mRNA. Cycloheximide abolished only the GFAP response to ethanol. This work shows that an interrelationship between ethanol and RA exists in the astrocyte.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Grummer MA,Salih ZN,Zachman RDdoi
10.1016/s0304-3940(00)01538-xkeywords:
subject
Has Abstractpub_date
2000-11-17 00:00:00pages
73-6issue
2eissn
0304-3940issn
1872-7972pii
S0304-3940(00)01538-Xjournal_volume
294pub_type
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