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.
GABAB receptors, which are part of the brain's inhibitory system, are modulated by accessory proteins called KCTD16. In experiments using mice lacking the KCTD16 gene, baseline pain sensitivity and nerve cell activity in the spinal cord were similar to normal mice. However, when treated with the GABAB receptor agonist baclofen, normal mice showed greater pain relief (higher thresholds for heat and touch) than mice lacking KCTD16. In a model of peripheral inflammation, KCTD16-deficient mice tended to have higher pain thresholds, and baclofen's inhibitory effect on nerve signals was reduced. The findings suggest KCTD16 may be important for pain modulation during pathological conditions when GABAB receptors are activated, but further research is needed.