Journal
ELIFE
Volume 9, Issue -, Pages -Publisher
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.53664
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Funding
- National Institute of Mental Health [R01MH112746]
- Wellcome [098830/Z/12/Z, 208789/Z/17/Z, 096689/Z/11/Z]
- Brain and Behavior Research Foundation
- National Institute for Health Research Oxford Health Biomedical Research Centre
- Middlesex Hospital Medical School General Charitable Trust
- NSERC [PGSD2 - 502866]
- Wellcome Trust [208789/Z/17/Z, 098830/Z/12/Z, 096689/Z/11/Z] Funding Source: Wellcome Trust
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Decision-making biases can be features of normal behaviour, or deficits underlying neuropsychiatric symptoms. We used behavioural psychophysics, spiking-circuit modelling and pharmacological manipulations to explore decision-making biases during evidence integration. Monkeys showed a pro-variance bias (PVB): a preference to choose options with more variable evidence. The PVB was also present in a spiking circuit model, revealing a potential neural mechanism for this behaviour. To model possible effects of NMDA receptor (NMDA-R) antagonism on this behaviour, we simulated the effects of NMDA-R hypofunction onto either excitatory or inhibitory neurons in the model. These were then tested experimentally using the NMDA-R antagonist ketamine, a pharmacological model of schizophrenia. Ketamine yielded an increase in subjects' PVB, consistent with lowered cortical excitation/inhibition balance from NMDA-R hypofunction predominantly onto excitatory neurons. These results provide a circuit-level mechanism that bridges across explanatory scales, from the synaptic to the behavioural, in neuropsychiatric disorders where decision-making biases are prominent.
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