Data from: A circuit mechanism for decision making biases and NMDA receptor hypofunction

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.