Chronic ethanol consumption increases the amount of mRNA for retinoic acid and triiodothyronine receptors in mouse brain

Neurosci Lett. 1996 Mar 15;206(2-3):73-6. doi: 10.1016/s0304-3940(96)12455-1.


It is known that alcohol induces disorders in the metabolism of retinoids and particularly in the biosynthetic pathways of retinoic acid (RA). Since RA has, along with other hormones and particularly triiodothyronine (T3), a physiological role in the adult brain, the effect of chronic exposure to alcohol on RA and T3 status was investigated. The amounts of RA receptor (RAR) and T3 receptor (TR) mRNAs were quantified and the activity of the 'tissue' transglutaminase (tTG; an RA-dependent enzyme) was assayed in the brain of mice following chronic ethanol consumption (CEC; 12% v/v for 6-10 months). Compared to controls, ethanol-treated mice exhibited increased amounts of RAR and TR mRNAs together with an increase in tTG activity. It is hypothesized that the enhanced cellular action of RA and T3 could play a role in the previously described brain damages induced by CEC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alcoholism / metabolism*
  • Animals
  • Base Sequence
  • Brain / drug effects*
  • Brain / metabolism
  • DNA-Directed RNA Polymerases / metabolism
  • Male
  • Mice
  • Molecular Sequence Data
  • RNA, Messenger / biosynthesis*
  • Random Allocation
  • Receptors, Retinoic Acid / genetics*
  • Receptors, Thyroid Hormone / genetics*


  • RNA, Messenger
  • Receptors, Retinoic Acid
  • Receptors, Thyroid Hormone
  • DNA-Directed RNA Polymerases