In the central nervous system (CNS), the c‐Jun transcription factor has been mainly studied in neuronal cells and coupled to apoptotic and regenerative pathways following brain injury. Besides, several studies have shown a transcriptional role of c‐Jun in activated cortical and spinal astrocytes. In contrast, little is known about c‐Jun expression and transactivation in Bergmann glial (BG) cells, the radial cerebellar astrocytes playing crucial roles in cerebellar development and physiology. Here, we used neuronal/glial cerebellar cultures from neonatal mice to assess putative functions of c‐Jun in BG cells. By performing double immunocytochemical staining of c‐Jun and two BG specific markers, S100 and glutamate aspartate transporter (GLAST), we show that c‐Jun was highly expressed in radial glial cells derived from Bergmann glia. Bergmann glia‐derived cells expressed toll‐like receptor 4 and treatment with bacterial lipopolysaccharide (LPS)‐induced c‐Jun phosphorylation at serine 63, a hallmark of c‐Jun transactivation, exclusively in BG cells. Moreover, LPS‐induced IL‐1β expression and inhibition of c‐Jun N‐terminal kinase (JNK) activity abolished both c‐Jun phosphorylation and the increase of IL‐1β mRNA. Notably, LPS failed to induce IL‐1β mRNA in neuronal/glial cerebellar cultures generated from conditional knockout mice lacking c‐Jun expression in the CNS, indicating the essential role of c‐Jun in astroglial‐specific induction of IL‐1β. Immunohistochemical analyses of c‐Jun‐expressing cells in the early postnatal cerebellum confirmed in vivo the expression of c‐Jun in BG cells and uncovered a dynamic expression of c‐Jun during the formation of the BG monolayer. Altogether, our finding underlines a putative role of c‐Jun in astroglia‐mediated neuroinflammatory dysfunctions of the cerebellum. © 2011 Wiley‐Liss, Inc.