| First Author | Hill MN | Year | 2011 |
| Journal | Cereb Cortex | Volume | 21 |
| Issue | 9 | Pages | 2056-64 |
| PubMed ID | 21263035 | Mgi Jnum | J:187351 |
| Mgi Id | MGI:5436223 | Doi | 10.1093/cercor/bhq280 |
| Citation | Hill MN, et al. (2011) Alterations in corticolimbic dendritic morphology and emotional behavior in cannabinoid CB1 receptor-deficient mice parallel the effects of chronic stress. Cereb Cortex 21(9):2056-64 |
| abstractText | Many changes produced by chronic stress are similar to those seen in cannabinoid CB(1) receptor-deficient mice. In the current study, we examined both anxiety-like behavior and dendritic complexity within the prefrontal cortex and basolateral amygdala (BLA) in wild-type and CB(1) receptor-deficient mice, under basal conditions and following exposure to 21 days of protracted restraint stress. CB(1) receptor-deficient mice exhibited increased indices of anxiety in the elevated plus maze under basal conditions that were similar in magnitude to changes seen in wild-type mice exposed to chronic stress. Chronic stress or deletion of the CB(1) receptor also produced a reduction in both apical dendritic length and branch points of neurons within layer II/III of the prelimbic region of the prefrontal cortex. Pyramidal neurons in the (BLA) of CB(1) receptor-deficient mice were found to have increased dendritic length compared with wild type. Chronic stress increased dendritic length of these amygdalar neurons in both wild-type and CB(1) receptor-deficient mice. Collectively, these data demonstrate that loss of cannabinoid CB(1) receptor signaling produces a chronic stress-like phenotype under basal conditions and provide a putative neural substrate that may subserve the changes in emotional behavior seen following disruption of CB(1) receptor signaling. |
