Alcohol use disorder (AUD) is a complex and severe neuropsychiatric disorder with high mortality and morbidity rates. Insight into the complex mechanisms that underlie alcohol-related responses would contribute toward novel treatment options for AUD. Glucagon-like peptide 1, a gut brain peptide that regulate appetite, has lately been suggested as such candidate. The GLP-1 receptor agonist, exendin-4 (Ex4), prevents alcohol-induced reward, alcohol intake, relapse drinking and the motivation to consume alcohol in rodents. However, the brain circuits that participate in the ability of GLP-1 to regulate alcohol-related responses is unknown. The paraventricular nucleus of thalamus (PVT) might serve as one candidate as it connects to nucleus accumbens, an area well known for its involvement in AUD processes. The hypothesis that activation of GLP-1 receptors, by means of local infusion of Ex4 into PVT, attenuates alcohol-related responses was tested in the present study. We showed that Ex4 into PVT attenuated alcohol-induced locomotor stimulation and dopamine release in nucleus accumbens of male mice. We further found that Ex4 into PVT decreased alcohol intake in male and female rats. Interestingly, female rats exhibited a higher dosage requirement than male rats, pointing to a gender-based variation in the GLP-1 response within the PVT. On the contrary, the expression of GLP-1 receptors showed no difference between high- and low-alcohol preferring rats. Taken together, these findings indicate that GLP-1 receptors expressed in the PVT play a role in alcohol-related responses, providing further evidence that targeting GLP-1 receptors could be a promising approach for AUD treatment.