Cbln1 is a member of the C1q and tomor necrosis factor superfamily. Cbln1 is predominantly expressed in the cerebellar granule cells. Cbln1, released from granule cells, is crucial for synapse formation and plasticity by binding to its receptor expressed in Purkinje cells. Recently, a null-mutation in the gene encoding GluD2 was reported to cause severe cognitive impairment in human. However it remained unclear whether the loss of Cbln1 also caused similar cognitive impairment, and if so, whether Cbln1-GluD2 signaling in the cerebellum was responsible for the phenotype because Cbln1 mRNA was also expressed in various forebrain regions, such as entorhinal cortex and retrosplenial granular cortex. To address these questions, we assessed non-motor functions Cbln1 knockout mice by conditioned fear learning test. Cbln1 knockout mice showed severe reduction in acquisition of the context and cued fear learning compared to control littermates. In addition, retention/recall was also severely affected in Cbln1 knockout mice at 10 min and 24 h after the conditioning. To determine whether Cbln1 expressed in the forebrain was responsible for this phenotype, we generated conditional Cbln1 knockout mice by crossing with CaMKIIa-Cre with floxed Cbln1 mice (CaMKIIa-Cre;Cbln1^f/f). Fear conditioning test revealed that although cue-dependent memories were intact, context-dependent fear memory retention were significantly impaired in CaMKIIa-Cre;Cbln1^f/f mice. Furthermore, spatial memory was assessed by water radial-arm maze test. CaMKIIa-Cre;Cbln1^f/f mice showed significant delay in learning of platform location compared with control mice. These result indicate Cbln1 expressed in the forebrain plays an essential role in non-motor associated learning.