| First Author | Lo SC | Year | 2015 |
| Journal | J Neurosci | Volume | 35 |
| Issue | 5 | Pages | 2118-32 |
| PubMed ID | 25653368 | Mgi Jnum | J:219897 |
| Mgi Id | MGI:5629916 | Doi | 10.1523/JNEUROSCI.3280-14.2015 |
| Citation | Lo SC, et al. (2015) Caspase-3 deficiency results in disrupted synaptic homeostasis and impaired attention control. J Neurosci 35(5):2118-32 |
| abstractText | The ability to attend to relevant stimuli and to adapt dynamically as demands change is a core aspect of cognition, and one that is impaired in several neuropsychiatric diseases, including attention deficit/hyperactivity disorder. However, the cellular and molecular mechanisms underlying such cognitive adaptability are poorly understood. We found that deletion of the caspase-3 gene, encoding an apoptosis protease with newly discovered roles in neural plasticity, disrupts attention in mice while preserving multiple learning and memory capabilities. Attention-related deficits include distractibility, impulsivity, behavioral rigidity, and reduced habituation to novel stimuli. Excess exploratory activity in Casp3(-/-) mice was correlated with enhanced novelty-induced activity in the dentate gyrus, which may be related to our findings that caspase-3 is required for homeostatic synaptic plasticity in vitro and homeostatic expression of AMPA receptors in vivo in response to chronic or repeated stimuli. These results suggest an important role for caspase-3 in synaptic suppression of irrelevant stimuli. |
