Ketamine, an NMDA receptor antagonist, disrupted electric signaling and navigation in the weakly electric fish Gnathonemus petersii, a candidate model for schizophrenia. Lower doses increased locomotion and erratic movement, while higher doses reduced electric organ discharges, indicating positive schizophrenia-like symptoms. A low dose of haloperidol did not normalize these symptoms, suggesting further testing with more antipsychotic doses is needed to confirm the model's predictive validity.
The weakly electric fish Gnathonemus petersii preferred a familiar object over a novel one in the novel object recognition task, spending less time, moving a shorter distance, and emitting fewer electric organ discharges when exploring the novel object. Ketamine, an NMDA receptor antagonist, did not produce significant behavioral changes on its own, and no direct link was found between electric organ discharges and behavioral responses to ketamine or typical antipsychotics. However, when ketamine was combined with the atypical antipsychotic clozapine, the fish no longer distinguished between the original and new objects, suggesting the drug combination disrupted object recognition.