| First Author | Jaehne EJ | Year | 2015 |
| Journal | Behav Brain Res | Volume | 281 |
| Pages | 276-82 | PubMed ID | 25549857 |
| Mgi Jnum | J:223967 | Mgi Id | MGI:5660708 |
| Doi | 10.1016/j.bbr.2014.12.044 | Citation | Jaehne EJ, et al. (2015) Effects of Npas4 deficiency on anxiety, depression-like, cognition and sociability behaviour. Behav Brain Res 281:276-82 |
| abstractText | The transcription factor neuronal PAS domain-containing protein 4 (Npas4), which regulates the formation of inhibitory synapses on excitatory neurons, has been suggested as a candidate gene for neurological and psychiatric conditions such as bipolar depression, autism spectrum and cognitive disorders. A mouse model of Npas4 deficiency has been developed to investigate any role in these disorders. Behavioural characterisation of Npas4(-/-), Npas4(+/-) and Npas4(+/+) mice has been conducted using the open field, elevated zero maze (EZM), Y-maze, sociability test and forced swim test (FST) to investigate a range of behaviours. Npas4(-/-) mice spent more time in the open arm of the EZM than other genotypes, suggesting decreased anxiety-like behaviour. Npas4(+/-) mice, however, were more immobile in the FST than other genotypes, suggesting increased depression-like behaviour, and also showed impaired spatial recognition memory in the Y-maze. There were no differences between genotype in social behaviour. These results suggest that differential levels of Npas4 expression in the brain may regulate anxiety, depression and cognition related disorders. |
