Pro-inflammatory cytokines can affect cognitive processes such as learning and memory. Particularly, interleukin-1β (IL-1β) influences hippocampus-dependent memories. We previously reported that administration of IL-1β in dorsal hippocampus impaired contextual fear memory reconsolidation. This effect was reversed by the melanocortin alpha-melanocyte-stimulating hormone (α-MSH). Our results also demonstrated that IL-1β produced a significant decrease in glutamate release from dorsal hippocampus synaptosomes after reactivation of the fear memory. Therefore, we investigated whether IL-1β administration can affect GluA1 AMPA subunit phosphorylation, surface expression, and total expression during reconsolidation of a contextual fear memory. Also, we studied the modulatory effect of α-MSH. We found that IL-1β reduced phosphorylation of this subunit at Serine 831 and Serine 845 60 min after contextual fear memory reactivation. The intrahippocampal administration of IL-1β after memory reactivation also induced a decrease in surface expression and total expression of GluA1. α-MSH prevented the effect of IL-1β on GluA1 phosphorylation in Serine 845, but not in Serine 831. Moreover, treatment with α-MSH also prevented the effect of the cytokine on GluA1 surface and total expression after memory reactivation. Our results demonstrated that IL-1β regulates phosphorylation of GluA1 and may thus play an important role in modulation of AMPAR function and synaptic plasticity in the brain. These findings further illustrate the importance of IL-1β in cognition processes dependent on the hippocampus, and also reinforced the fact that α-MSH can reverse IL-1β effects on memory reconsolidation.