Schizophrenia is a devastating psychiatric illness with a complex pathophysiology. We have recently documented schizophrenia‐like endophenotypes in phospholipase C‐β1 knockout (PLC‐β1^−/−) mice, including deficits in prepulse inhibition, hyperlocomotion, and cognitive impairments. PLC‐β1 signals via multiple G‐protein coupled receptor pathways implicated in neural cellular plasticity; however, adult neurogenesis has yet to be explored in this knockout model. In this study, weemployed PLC‐β1^−/− mice to elucidate possible correlates between aberrant adult hippocampal neurogenesis (AHN) and schizophrenia‐like behaviors. Using stereology and bromodeoxyuridine (BrdU) immunohistochemistry we demonstrated a significant increase in the density of adult‐generated cells in the granule cell layer (GCL) of adult PLC‐β1^−/− mice compared with wild‐type littermates. Cellular phenotype analysis using confocal microscopy revealed these cells to be mature granule neurons expressing NeuN and calbindin. Increased neuronal survival occurred concomitant with reduced caspase‐3(+) cells in the GCL of PLC‐β1^−/− mice. Stereological analysis of Ki67(+) cells in the subgranular zone suggested that neural precursor proliferation is unchanged in PLC‐β1^−/− mice. We further showed aberrant migration of mature granule neurons within the GCL of adult PLC‐β1^−/− mice with excessive adult‐generated mature neurons residing in the middle and outer GCL. PLC‐β1^−/− mice exhibited specific behavioral deficits in location recognition, a measure of hippocampal‐dependent memory, but not novel object recognition. Overall, we have shown that PLC‐β1^−/− mice have a threefold increase in net AHN, and have provided further evidence to suggest a specific deficit in hippocampal‐dependent cognition. We propose that abnormal cellular plasticity in these mice may contribute to their schizophrenia‐like behavioral endophenotypes. © 2010 Wiley Periodicals, Inc.