| First Author | Chen X | Year | 2015 |
| Journal | J Neurosci | Volume | 35 |
| Issue | 1 | Pages | 339-51 |
| PubMed ID | 25568126 | Mgi Jnum | J:217730 |
| Mgi Id | MGI:5615511 | Doi | 10.1523/JNEUROSCI.2478-14.2015 |
| Citation | Chen X, et al. (2015) Overexpression of the type 1 adenylyl cyclase in the forebrain leads to deficits of behavioral inhibition. J Neurosci 35(1):339-51 |
| abstractText | The type 1 adenylyl cyclase (AC1) is an activity-dependent, calcium-stimulated adenylyl cyclase expressed in the nervous system that is implicated in memory formation. We examined the locomotor activity, and impulsive and social behaviors of AC1+ mice, a transgenic mouse strain overexpressing AC1 in the forebrain. Here we report that AC1+ mice exhibit hyperactive behaviors and demonstrate increased impulsivity and reduced sociability. In contrast, AC1 and AC8 double knock-out mice are hypoactive, and exhibit increased sociability and reduced impulsivity. Interestingly, the hyperactivity of AC1+ mice can be corrected by valproate, a mood-stabilizing drug. These data indicate that increased expression of AC1 in the forebrain leads to deficits in behavioral inhibition. |
