NEUROPEPTIDE-Y LEVELS IN ETHANOL-NAIVE, ALCOHOL-PREFERRING, AND NONPREFERRING RATS AND IN WISTAR RATS AFTER ETHANOL EXPOSURE

Citation
Cl. Ehlers et al., NEUROPEPTIDE-Y LEVELS IN ETHANOL-NAIVE, ALCOHOL-PREFERRING, AND NONPREFERRING RATS AND IN WISTAR RATS AFTER ETHANOL EXPOSURE, Alcoholism, clinical and experimental research, 22(8), 1998, pp. 1778-1782
Citations number
48
Categorie Soggetti
Substance Abuse
ISSN journal
01456008
Volume
22
Issue
8
Year of publication
1998
Pages
1778 - 1782
Database
ISI
SICI code
0145-6008(1998)22:8<1778:NLIEAA>2.0.ZU;2-7
Abstract
Neuropeptide Y (NPY) is a hexatriacontapeptide amide that is now well characterized as a neuromodulator in the central nervous system (CNS), When infused into the CNS, NPY produces both anxiolytic end orexigeni c effects. NPY's anxiolytic effects appear to be mediated through rece ptors in the central amygdala, whereas its orexigenic effects are loca lized in discrete hypothalamic nuclei. Both food restriction and food deprivation produce increased revels of the peptide in the hypothalamu s that are ameliorated by refeeding. However, the effects of alcohol c onsumption/deprivation on NPY levels remain unknown. The present study sought to determine if brain NPY levels were affected by either alcoh ol exposure and/or correlated with genetic differences in preference f or drinking alcohol. In the first experiment, NPY-like immunoreactivit y (NPY-LI) was compared in alcohol-naive, alcohol-preferring (P), and nonpreferring (NP) rats. After tissue extraction, NPY-LI was measured by radioimmunoassay: amygdala, hippocampus, frontal cortex, hypothalam us, and caudate. P rats were found to have significantly lower NPY-LI in amygdala (F = 4.69, p < 0.04), hippocampus (F = 7.03, p < 0.01), an d frontal cortex (F = 4.7, p < 0.04), compared with NP rats. In the se cond experiment, heterozygous Wistar rats were exposed to alcohol for 14 hr/day for 7 weeks in alcohol vapor chambers (mean blood alcohol co ncentrations = 180 mg%) or control chambers. At 7 weeks of alcohol exp osure, no significant changes in NPY-LI in were found. At 1 month afte r ethanol withdrawal, however, the ethanol-exposed animals had signifi cantly higher NPY-LI in the hypothalamus (F = 4.78, p < 0.04) when com pared with the nonexposed controls. Taken together, these studies sugg est that exposure to chronic ethanol may affect NPY-LI at the level of the hypothalamus in a fashion similar to food restriction, because 4 weeks after alcohol withdrawal, significantly higher NPY levels are fo und. In addition, differences in NPY-LI in limbic areas and frontal co rtex between alcohol-naive P and NP rats suggest that NPY may also pla y a role in risk for the development of alcohol preference either by m odulating the ''tension-reduction'' properties of alcohol or by influe ncing consummatory behaviors.