Effects of chronic ethanol consumption and aging on proenkephalin and neurotensin

We examined the combined effects of chronic ethanol consumption and aging on mRNA and peptide for proenkephalin (PE), the precursor of met- and leu-enkephalin. This study also evaluated the effects of aging and alcohol on the level of the mRNA encoding the common precursor of neurotensin (NT) and neuromedin N (NN). PE mRNA and NT/NN mRNA were quantitated in multiple brain areas of 5- and 24-month-old male Fischer 344 rats. Aging, but not chronic ethanol consumption, altered PE mRNA and peptide levels. Aging was accompanied by a loss of PE peptide and PE mRNA in the rostral striatum. In aged rats, PE mRNA was also reduced in the shell region of the nucleus accumbens. The decline in PE mRNA in the rostral striatum and shell region of the nucleus accumbens was caused by a reduction in the number of cells that contain PE mRNA. The percentage of PE mRNA-containing neurons that express a high amount of PE mRNA was also lower in the rostral striatum of 24-month-old rats. The effects of aging may impair motor function and alter the rewarding properties of ethanol consumption. Neither aging nor alcohol changed the PE mRNA levels in the core region of the nucleus accumbens, the frontal cortex, and the piriform cortex. In contrast to PE mRNA, neither aging nor chronic ethanol consumption affected NT/NN mRNA in the regions analyzed. Normal NT/NN mRNA levels were found in the lateral septum and two hippocampal brain areas: the dorsal subiculum and CA1 regions.