Cognitive deficits in the Snord116 deletion mouse model for Prader-Willi syndrome

•A lack of the gene cluster SNORD116 may be responsible for some aspects of PWS.•Heterozygous Snord116 mutation mice had learning and memory deficits in three assays.•Heterozygous deletions in Snord116 did not impair exploratory or motor abilities.•Snord116+/− model is a valuable preclinical tool for investigating PWS.