TY - JOUR
T1 - Model based control can give rise to devaluation insensitive choice
AU - Garrett, Neil
AU - Allan, Sean
AU - Daw, Nathaniel D.
N1 - Publisher Copyright:
© 2023
PY - 2023/6
Y1 - 2023/6
N2 - Influential recent work aims to ground psychiatric dysfunction in the brain's basic computational mechanisms. For instance, the compulsive symptoms that feature prominently in drug abuse and addiction have been argued to arise from over reliance on a habitual “model-free” system in contrast to a more laborious “model-based” system. Support for this account comes in part from failures to appropriately change behavior in light of new events. Notably, instrumental responding can, in some circumstances, persist despite reinforcer devaluation, perhaps reflecting control by model-free mechanisms that are driven by past reinforcement rather than knowledge of the (now devalued) outcome. However, another line of theory posits a different mechanism – latent causal inference – that can modulate behavioral change. It concerns how animals identify different contingencies that apply in different circumstances, by covertly clustering experiences into distinct groups. Here we combine both lines of theory to investigate the consequences of latent cause inference on instrumental sensitivity to reinforcer devaluation. We show that instrumental insensitivity to reinforcer devaluation can arise in this theory even using only model-based planning, and does not require or imply any habitual, model-free component. These ersatz habits (like laboratory ones) emerge after overtraining, interact with contextual cues, and show preserved sensitivity to reinforcer devaluation on a separate consumption test, a standard control. Together, this work highlights the need for caution in using reinforcer devaluation procedures to rule in (or out) the contribution of different learning mechanisms and offers a new perspective on the neurocomputational substrates of drug abuse.
AB - Influential recent work aims to ground psychiatric dysfunction in the brain's basic computational mechanisms. For instance, the compulsive symptoms that feature prominently in drug abuse and addiction have been argued to arise from over reliance on a habitual “model-free” system in contrast to a more laborious “model-based” system. Support for this account comes in part from failures to appropriately change behavior in light of new events. Notably, instrumental responding can, in some circumstances, persist despite reinforcer devaluation, perhaps reflecting control by model-free mechanisms that are driven by past reinforcement rather than knowledge of the (now devalued) outcome. However, another line of theory posits a different mechanism – latent causal inference – that can modulate behavioral change. It concerns how animals identify different contingencies that apply in different circumstances, by covertly clustering experiences into distinct groups. Here we combine both lines of theory to investigate the consequences of latent cause inference on instrumental sensitivity to reinforcer devaluation. We show that instrumental insensitivity to reinforcer devaluation can arise in this theory even using only model-based planning, and does not require or imply any habitual, model-free component. These ersatz habits (like laboratory ones) emerge after overtraining, interact with contextual cues, and show preserved sensitivity to reinforcer devaluation on a separate consumption test, a standard control. Together, this work highlights the need for caution in using reinforcer devaluation procedures to rule in (or out) the contribution of different learning mechanisms and offers a new perspective on the neurocomputational substrates of drug abuse.
KW - Addiction
KW - Devaluation
KW - Habits
KW - Latent causal inference
KW - Model based planning
UR - http://www.scopus.com/inward/record.url?scp=85174666077&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85174666077&partnerID=8YFLogxK
U2 - 10.1016/j.addicn.2023.100070
DO - 10.1016/j.addicn.2023.100070
M3 - Article
AN - SCOPUS:85174666077
SN - 2772-3925
VL - 6
JO - Addiction Neuroscience
JF - Addiction Neuroscience
M1 - 100070
ER -