GABAergic neurotransmission is enhanced in the cerebellum of hyperammonemic rats, an animal model of hepatic encephalopathy, and this induces motor incoordination. There is an interplay between neuroinflammation and GABAergic neurotransmission, but the underlying mechanisms remain unclear. This work aimed to unveil the molecular mechanisms by which GABAergic neurotransmission modulates neuroinflammation in the cerebellum.Ex-vivo experiments were performed using cerebellar slices from control and hyperammonemic rats treated or not with bicuculline. We analyzed by immunohistochemistry microglia perimeter and astrocytes area, measures of glial activation, to assess the effects on neuroinflammation. Other mechanisms by which bicuculline may modulate neuroinflammation include the nuclear localization of the pro-inflammatory transcription factor NF-κβ, which was assessed by immunofluorescence. The content of proinflammatory factors and the membrane expression of key proteins was also analyzed by Western-blot.We found that treatment with bicuculline reverses astrocytes but not microglia activation in the cerebellum of hyperammonemic rats. Bicuculline reverses the nuclear translocation of p50 subunit of NF-κβ in Purkinje cells, which is enhanced in hyperammonemia. It also reverses the increase of some pro-inflammatory proteins such as IL-1β, IL-6 or TNFα. These results prove that bicuculline reduces neuroinflammation in cerebellum of hyperammonemic rats, and provides clues about the molecular mechanisms underlying the modulation by GABAergic neurotransmission of neuroinflammation.Neuroinflammation in cerebellum is responsible for the impairment of motor coordination in hyperammonemia and hepatic encephalopathy. The data reported suggest that treatments reducing GABAergic neurotransmission may be a therapeutic approach to improve these symptoms in patients with hepatic encephalopathy.