This study was supported by the National Institute of Alcohol Abuse and Alcoholism Grants AA 00223 and AA 06059 to C.L.E., Grant AA 07611 to T-K. Li, and by a grant from the Karolinska Institute and the Swedish Medical Research Council 10414 to A.A.M. This research was presented in part at the 1997 ACNP meeting.
Neuropeptide Y Levels in Ethanol-Naive Alcohol-Preferring and Nonpreferring Rats and in Wistar Rats after Ethanol Exposure
Article first published online: 30 MAY 2006
Alcoholism: Clinical and Experimental Research
Volume 22, Issue 8, pages 1778–1782, November 1998
How to Cite
Ehlers, C. L., Li, T.-K., Lurneng, L., Hwang, B. H., Somes, C., Jimenez, P. and Mathé, A. A. (1998), Neuropeptide Y Levels in Ethanol-Naive Alcohol-Preferring and Nonpreferring Rats and in Wistar Rats after Ethanol Exposure. Alcoholism: Clinical and Experimental Research, 22: 1778–1782. doi: 10.1111/j.1530-0277.1998.tb03979.x
- Issue published online: 30 MAY 2006
- Article first published online: 30 MAY 2006
- Received for publication March 18. 1998; accepted July 8, 1998
- Alcohol-Preferring Rats;
- Neuropeptide Y (NPY);
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 and orexigenic effects. NPY's anxiolytic effects appear to be mediated through receptors in the central amygdala, whereas its orexigenic effects are localized in discrete hypothalamic nuclei. Both food restriction and food deprivation produce increased levels of the pep-tide in the hypothalamus that are ameliorated by refeeding. However, the effects of alcohol consumption/deprivation on NPY levels remain unknown. The present study sought to determine if brain NPY levels were affected by either alcohol exposure and/or correlated with genetic differences in preference for drinking alcohol. In the first experiment, NPY-like immunoreactivity (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, hypothalamus, 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), and frontal cortex (F= 4.7, p < 0.04), compared with NP rats. In the second experiment, heterozygous Wistar rats were exposed to alcohol for 14 hr/day for 7 weeks in alcohol vapor chambers (mean blood alcohol concentrations =180 mg%) or control chambers. At 7 weeks of alcohol exposure, no significant changes in NPY-LI in were found. At 1 month after ethanol withdrawal, however, the ethanol-exposed animals had significantly higher NPY-LI in the hypothalamus (F= 4.78, p < 0.04) when compared with the nonexposed controls. Taken together, these studies suggest 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 found. In addition, differences in NPY-LI in limbic areas and frontal cortex between alcohol-naive P and NP rats suggest that NPY may also play a role in risk for the development of alcohol preference either by modulating the “tension-reduction” properties of alcohol or by influencing consummatory behaviors.