| First Author | Hamm JP | Year | 2017 |
| Journal | Neuron | Volume | 94 |
| Issue | 1 | Pages | 153-167.e8 |
| PubMed ID | 28384469 | Mgi Jnum | J:253243 |
| Mgi Id | MGI:6109157 | Doi | 10.1016/j.neuron.2017.03.019 |
| Citation | Hamm JP, et al. (2017) Altered Cortical Ensembles in Mouse Models of Schizophrenia. Neuron 94(1):153-167.e8 |
| abstractText | In schizophrenia, brain-wide alterations have been identified at the molecular and cellular levels, yet how these phenomena affect cortical circuit activity remains unclear. We studied two mouse models of schizophrenia-relevant disease processes: chronic ketamine (KET) administration and Df(16)A(+/-), modeling 22q11.2 microdeletions, a genetic variant highly penetrant for schizophrenia. Local field potential recordings in visual cortex confirmed gamma-band abnormalities similar to patient studies. Two-photon calcium imaging of local cortical populations revealed in both models a deficit in the reliability of neuronal coactivity patterns (ensembles), which was not a simple consequence of altered single-neuron activity. This effect was present in ongoing and sensory-evoked activity and was not replicated by acute ketamine administration or pharmacogenetic parvalbumin-interneuron suppression. These results are consistent with the hypothesis that schizophrenia is an "attractor" disease and demonstrate that degraded neuronal ensembles are a common consequence of diverse genetic, cellular, and synaptic alterations seen in chronic schizophrenia. |