Journal
NEURON
Volume 77, Issue 6, Pages 1151-1162Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2013.01.038
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Funding
- NINDS
- Anonymous Foundation
- NARSAD
- International Mental Health Research Organization
- Hope for Depression Research Foundation
- NIH [R21 MH093887, R01 MH081968, U19MH82441]
- Fondation Fyssen Fellowship
- [R25 MH086466]
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Cognitive deficits are central to schizophrenia, but the underlying mechanisms still remain unclear. Imaging studies performed in patients point to decreased activity in the nnediodorsal thalamus (MD) and reduced functional connectivity between the MD and prefrontal cortex (PFC) as candidate mechanisms. However, a causal link is still missing. We used a pharmacogenetic approach in mice to diminish MD neuron activity and examined the behavioral and physiological consequences. We found that a subtle decrease in MD activity is sufficient to trigger selective impairments in prefrontal-dependent cognitive tasks. In vivo recordings in behaving animals revealed that MD-PFC beta-range synchrony is enhanced during acquisition and performance of a working memory task. Decreasing MD activity interfered with this task-dependent modulation of MD-PFC synchrony, which correlated with impaired working memory. These findings suggest that altered MD activity is sufficient to disrupt prefrontal-dependent cognitive behaviors and could contribute to the cognitive symptoms observed in schizophrenia.
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