Recent research has highlighted a potential role for neuropeptide Y (NPY) and its Y 1 receptor in the development of schizophrenia. Genetic as well as molecular biological studies have demonstrated reduced levels of NPY in schizophrenia patients. Importantly, Y 1 receptors may mediate some of the potential effects of NPY on schizophrenia, as decreased Y 1 receptor expression has been found in the lymphocytes of schizophrenia patients. To clarify NPY’s role in schizophrenia, we investigated a genetic animal model for Y 1 deficiency in regard to (i) acoustic startle response (ASR), (ii) habituation to ASR and (iii) sensorimotor gating [i.e. prepulse inhibition (PPI)] using two different PPI protocols. Mutant and wild type-like mice were screened for baseline behaviours and after pharmacological challenge with the psychotropic drugs dexamphetamine (DEX) and MK-801. Y 1 knockout mice (Y 1 −/− ) showed a moderate reduction of the ASR and an impaired ASR habituation at baseline and after DEX treatment. The baseline PPI performance of Y 1 mutant mice was unaltered their response to DEX and MK-801 challenge was moderately different compared to control mice, which was dependent on the PPI protocol used. MK-801 challenge had a protocol-dependent differential effect in Y 1 −/− mice and DEX a more pronounced impact at the highest prepulse intensities. In conclusion, it appears that the Y 1 receptor influences the acoustic startle response and its habituation but does not play a major role in sensorimotor gating. Further explorations into the effects of Y 1 deficiency seem valid.