Prepulse inhibition (PPI) is the phenomenon in which a weak prepulse stimulus attenuates the response to a subsequent startling stimulus. Patients with schizophrenia and some other neuropsychiatric disorders have impaired PPI. Impaired PPI in these patient populations is thought to reflect dysfunctional sensorimotor gating mechanisms. Recently, various inbred mouse strains and genetically modified mouse lines have been examined to investigate the potential genetic basis of sensorimotor gating. This review provides a synopsis of the use of mouse models to explore genetic and neurochemical influences on PPI. Studies describing the PPI responses of various inbred strains of mice, mice with genetic mutations, and mice treated with various drugs prior to July 2001 are reviewed. The continuous nature of the distribution of PPI responses among inbred strains of mice indicates that PPI is a polygenic trait. Findings from spontaneous and gene-targeted mutants suggest that mutant mice are important tools for dissecting and studying the role of single genes and their products, and chromosomal regions in regulating PPI. Pharmacological studies of PPI have typically confirmed effects in mice that are similar to those reported previously in rats, with some important exceptions. The use of mice to study PPI is increasing at a dramatic rate and is helping to increase our understanding of the biological basis for sensorimotor gating.