An amphetamine study found related reward-evoked electrical responses in humans and mice, but the frequency-domain effects differed. Cross-species similarity was partial, not evidence that every neural measure responded identically.
Cavanagh and colleagues studied reward processing during a probabilistic learning task in 23 humans and 28 mice. Human conditions included placebo and d-amphetamine 10 and 20 mg; mouse conditions used saline or several weight-adjusted doses. EEG analyses examined event-related potentials and spectral activity, which describe different properties of the electrical response.
In humans, amphetamine increased the Reward Positivity component and its delta-band representation. In mice, it increased reward- and punishment-related potential features without significantly modulating the spectral measures. The behavioral task results did not show a corresponding universal learning benefit. A stronger electrical response to an outcome cannot simply be renamed better learning or better decisions.
The drug affects more than dopamine, so the experiment did not isolate a single transmitter as the exclusive cause of the signal changes. Species also differed in their discrimination of task probabilities. These considerations limit mechanistic claims and the strength of the translation. A candidate biomarker can be sensitive to a drug without being a validated predictor of clinical response. The study did not assess individual intoxication, drug identification or driving. Its value is testing which components of a proposed reward measure are pharmacologically sensitive, while preserving the species-specific null findings that constrain a broad common-mechanism account.
See the difference between a mechanistic signal and a clinical treatment result.