Abstract
Learning deficit is a clinical feature of many mental disorders and is hypothesized to result from an inability to integrate information in neural systems. We showed that transgenic mice expressing a dominant-negative form of DISC1, a risk gene for neuropsychiatric disorders, exhibited impaired performance in a reward-place association task when combined with a mild isolation stress. CA1 cells in the mutant mice showed normal place cell properties, but their activity at the goal zone was diminished. This abnormality in hippocampal activity at the goal zone during the task may underlie the learning deficit observed in the DISC1 mutant mice.
Original language | English (US) |
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Pages (from-to) | 70-73 |
Number of pages | 4 |
Journal | Neuroscience Research |
Volume | 106 |
DOIs | |
State | Published - May 1 2016 |
Keywords
- DISC1
- Hippocampus
- Learning deficit
- Mental disorder
- Neural activity
- Reward
ASJC Scopus subject areas
- Neuroscience(all)