Different alcohol drinking patterns, involving either small and frequent 
drinking bouts or large and long-lasting bouts, are found to differentially 
affect the risk for developing alcohol-related diseases, suggesting that they 
have different underlying mechanisms. Such mechanisms may involve orexigenic 
peptides known to stimulate alcohol intake through their actions in the 
hypothalamic paraventricular nucleus (PVN). These include orexin (OX), which is 
expressed in the perifornical lateral hypothalamus, and galanin (GAL) and 
enkephalin (ENK), which are expressed within as well as outside the PVN. To 
investigate the possibility that these peptides affect different aspects of 
consumption, a microstructural analysis of ethanol drinking behavior was 
performed in male, Sprague-Dawley rats trained to drink 7% ethanol and implanted 
with guide shafts aimed at the PVN. While housed in specialized cages containing 
computerized intake monitors (BioDAQ Laboratory Intake Monitoring System, 
Research Diets Inc., New Brunswick, NJ) that measure bouts of ethanol drinking, 
these rats were given PVN injections of OX (0.9 nmol), GAL (1.0 nmol), or the 
ENK analog D-Ala2-met-enkephalinamide (DALA) (14.2 nmol), as compared to saline 
vehicle. Results revealed clear differences between the effects of these 
peptides. While all 3 stimulated ethanol intake, they had distinct effects on 
patterns of drinking, with OX increasing the number of drinking bouts, GAL 
increasing the size of the drinking bouts, and DALA increasing both the size and 
duration of the bouts. In contrast, these peptides had little impact on water or 
food intake. These results support the idea that different peptides can increase 
ethanol consumption by promoting distinct aspects of the ethanol drinking 
response. The stimulatory effect of OX on drinking frequency may be related to 
its neuronally stimulatory properties, while the stimulatory effect of GAL and 
ENK on bout size and duration may reflect a suppressive effect of these 
neuronally inhibitory peptides on the satiety-controlling PVN.