| First Author | Fang C | Year | 2012 |
| Journal | Neuroscience | Volume | 218 |
| Pages | 170-80 | PubMed ID | 22626646 |
| Mgi Jnum | J:192427 | Mgi Id | MGI:5465071 |
| Doi | 10.1016/j.neuroscience.2012.05.027 | Citation | Fang C, et al. (2012) Neurobehavioral abnormalities in a brain-specific NADPH-cytochrome P450 reductase knockout mouse model. Neuroscience 218:170-80 |
| abstractText | The aim of the present study was to test a new hypothesis that brain cytochrome P450 reductase (CPR) and CPR-dependent enzymes play important roles in behavioral performance. A mouse model with brain neuron-specific deletion of the Cpr gene (brain-Cpr-null) was recently generated. Brain-Cpr-null mice and wild-type (WT) littermates were compared in a variety of behavioral assays. Notable differences were found in the exploratory behavior assay: for both males and females, activity in the center of the chamber was significantly higher for brain-Cpr-null than for WT mice on days 2 and 3 of the assay, although no significant difference was found between the two groups in anxiety-like behavior in the elevated zero maze. Furthermore, in the fear-conditioning assay, brain-Cpr-null mice exhibited significantly less activity suppression than did WT controls. This deficit in activity suppression was not accompanied by any difference between WT and brain-Cpr-null mice in nociceptive responses to foot shocks. Abnormal activity suppression was also observed in both male and female brain-Cpr-null mice during the contextual memory test. However, in the Morris water maze assay, the brain-Cpr-null and WT mice were indistinguishable, indicating normal spatial memory in the mutant mice. These data collectively indicate a novel role of the Cpr gene in fear conditioning and memory. |
