| Abstract | Midlatency event-related potentials (ERPs) reflect early stages in processing of modality specific information. In humans, the auditory midlatency ERPs most investigated are the P1, N1 and P2. Abnormalities of these ERPs in neuropsychiatric disorders such as schizophrenia point to deficits in information processing at early stages. Investigations of corresponding ERPs in mice might thus permit to elucidate the molecular biology of such abnormalities. We conducted studies in mice and humans in order to establish the correspondence of midlatency ERPs in mice to the human P1, N1 and P2. We investigated their so-called recovery function-i.e. their systematic amplitude changes as a function of varying stimulus onset asynchrony (SOA). Furthermore, we explored effects of specific genetic alterations (ERK1 gene deletion GDI1 gene deletion) on this measure. In mice, P1-like activity showed a significant recovery not present in human data. In contrast, N1-like and P2-like activity in mice demonstrated similar recovery functions as the corresponding ERPs in human subjects and could be best fitted by the same function. In addition, ERK1 gene knockout mice showed a significantly different N1 recovery function compared to wild-type mice, possibly related to enhanced memory functions in these mice. Our results indicate that midlatency ERPs in mice share some, but not all, characteristics with the human P1, N1 and P2. As in humans, N1 recovery may provide an assessment of auditory sensory memory function. Investigations of these ERPs in mice may thus permit to elucidate the abnormalities underlying deficient generation of these ERPs in neuropsychiatric disorders. |