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Introduction
In the previous post, we examined how tonic dopamine shapes motivation, curiosity, and behavioral vigor. We saw that different motivational regimes — apathy, healthy goal pursuit, compulsion, and oscillatory instability — emerge from the interaction between tonic dopamine and hedonic adaptation.
However, none of those regimes produced addiction.
The agent never pursued the target in the absence of pleasure.
It never developed persistent attraction to neutral stimuli.
It never exhibited craving.
This limitation was intentional.
To understand addiction-like behavior, we must introduce a second dopaminergic dynamic: phasic dopamine.
While tonic dopamine energizes behavior globally, phasic dopamine encodes rapid, transient bursts linked to reward prediction errors. In this post, we extend the previous model by adding phasic dopamine and cue sensitization — and examine how addiction-like dynamics emerge.
Conceptual framing
The extended model preserves all assumptions from the tonic dopamine simulation, including:
An interoceptive hedonic target.
Hedonic adaptation via exponential decay of target gain.
Tonic dopamine (DATonic) scaling global motivational vigor.
The critical additions are:
A cue colocated with the target.
A phasic dopamine burst (DAPhasic) triggered upon unexpected reward.
A sensitization mechanism, whereby repeated phasic bursts increase the gain of the cue representation.
In this framework:
DATonic scales overall motivation.
DAPhasic updates the salience of specific states.
Addiction emerges when cue salience persists despite declining hedonic value.
The extended simulated environment
The environment is identical to the previous simulation, with one addition:
A neutral cue is colocated with the hedonic target.
Initially:
The cue has no or little initial intrinsic value.
It merely marks the spatial location of reward.
Over time:
Phasic dopamine bursts strengthen the cue’s salience.
This creates a divergence between:
Hedonic value (which decays),
Cue salience (which can increase).
Phasic dopamine as reward prediction error
Phasic dopamine bursts are modeled as transient increases triggered when:
This mechanism produces incentive sensitization.
Crucially, hedonic adaptation continues independently.
Dissociation between “liking” and “wanting”
As the agent repeatedly reaches the target:
Hedonic value decays exponentially.
Cue salience increases incrementally.
Eventually:
Pleasure decreases.
Cue-driven motivation increases.
This produces a state where:
The agent strongly “wants” what it increasingly fails to “like.”
This is the computational signature of addiction.
Emergent behavioral regimes
As in the tonic dopamine model, distinct regimes emerge from parameter interactions.
Here, the key dimensions are:
DATonic (global motivation)
Cue sensitization rate (α)
Hedonic adaptation rate
(a) Low sensitization
If cue gain increases, but remains low:
Behavior resembles the tonic dopamine regimes.
No addiction occurs.
Hedonic decay eventually extinguishes pursuit.
This replicates the previous post’s findings.
(b) Strong sensitization
Observed behavior:
Agent continues to approach the cue even after hedonic value declines to negligible values.
Seeking becomes decoupled from pleasure.
Reduced behavioral flexibility.
Interpretation:
Full addiction-like behavior.
Cue-driven motivation dominates.
Cue salience overrides hedonic feedback.
Figure 1. Divergence of hedonic value and cue gain.
Caption:
The hedonic target (blue) is colocated with a neutral cue. Phasic dopamine bursts occur when the agent unexpectedly receives reward, increasing cue salience. Hedonic value decays with repeated consumption, while cue gain increases through phasic dopamine bursts, producing dissociation between liking and wanting. However, since cue salience remains low, no addiction is observed.
Figure 2. Addiction-like regime.
Caption:
Persistent approach behavior driven by cue salience, despite declining hedonic value.
Comparison with tonic dopamine regimes
The contrast with the previous post is illuminating:
| Tonic-only model | Phasic-extended model |
|---|---|
| Motivation tied to hedonic value | Motivation can decouple from hedonic value |
| No persistent seeking without pleasure | Persistent seeking despite low pleasure |
| Compulsion without addiction | Cue-driven addiction-like behavior |
Tonic dopamine energizes behavior.
Phasic dopamine assigns salience.
Addiction requires both.
Why tonic dopamine alone cannot produce addiction
In the tonic-only model:
Motivation collapses when hedonic value decays.
No cue becomes intrinsically attractive.
Behavior remains tied to interoceptive reward.
Therefore:
Tonic dopamine explains vigor, not craving.
Only when phasic dopamine strengthens cue representations does persistent seeking emerge.
Addiction as maladaptive precision
In active inference terms, addiction can be interpreted as:
Excessively precise priors over cue-related policies.
Overweighting of exteroceptive salience.
Reduced influence of interoceptive negative feedback.
This reframes addiction as a disorder of precision weighting rather than simple reward excess.
What this model does not explain
This minimal model does not include:
Withdrawal states,
Stress modulation,
Trauma interactions,
Noradrenergic arousal systems.
These elements are critical in real addiction and will require further extensions.
Looking ahead
In the next step of this research, we will explore how threat, arousal, and avoidance systems interact with dopaminergic motivation.
If phasic dopamine explains why we pursue cues despite declining pleasure, understanding trauma will require modeling how certain cues become associated not with reward, but with threat — and how avoidance becomes compulsive.
Addiction and trauma may ultimately emerge as dual pathologies of precision in opposite motivational directions.
Conclusion
By extending the tonic dopamine model to include phasic bursts and cue sensitization, we observe the emergence of addiction-like dynamics.
The critical mechanism is not increased pleasure, but the divergence between:
hedonic value (which declines),
and cue salience (which increases).
This dissociation between liking and wanting transforms motivated behavior into persistent, inflexible seeking.
Tonic dopamine energizes behavior.
Phasic dopamine reshapes what behavior is directed toward.
Together, they form the computational backbone of addiction.
