| First Author | Martyn AC | Year | 2018 |
| Journal | PLoS One | Volume | 13 |
| Issue | 3 | Pages | e0194350 |
| PubMed ID | 29554125 | Mgi Jnum | J:259711 |
| Mgi Id | MGI:6148602 | Doi | 10.1371/journal.pone.0194350 |
| Citation | Martyn AC, et al. (2018) GIT1 regulates synaptic structural plasticity underlying learning. PLoS One 13(3):e0194350 |
| abstractText | The signaling scaffold protein GIT1 is expressed widely throughout the brain, but its function in vivo remains elusive. Mice lacking GIT1 have been proposed as a model for attention deficit-hyperactivity disorder, due to alterations in basal locomotor activity as well as paradoxical locomotor suppression by the psychostimulant amphetamine. Since we had previously shown that GIT1-knockout mice have normal locomotor activity, here we examined GIT1-deficient mice for ADHD-like behavior in more detail, and find neither hyperactivity nor amphetamine-induced locomotor suppression. Instead, GIT1-deficient mice exhibit profound learning and memory defects and reduced synaptic structural plasticity, consistent with an intellectual disability phenotype. We conclude that loss of GIT1 alone is insufficient to drive a robust ADHD phenotype in distinct strains of mice. In contrast, multiple learning and memory defects have been observed here and in other studies using distinct GIT1-knockout lines, consistent with a predominant intellectual disability phenotype related to altered synaptic structural plasticity. |
