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Ketamine disrupts locomotion and electrolocation in a novel model of schizophrenia, Gnathonemus petersii fish

Veronika Langová, Petra Horká, Jan Hubený, Tomáš Novák, Karel Valeš, Petr Adámek, Kateřina Holubová, Jiřı́ Horáček

Journal of Neuroscience Research March 3, 2023 DOI: 10.1002/jnr.25186 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Experimental study Peer reviewed
Population Weakly electric fish Gnathonemus petersii
Interventions Ketamine Haloperidol
Topics Ketamine Esketamine
Keywords Electroreception Schizophrenia object-oriented programming Fish <actinopterygii> Communication Fishery
Citations 10
Key findings Ketamine induced positive schizophrenia-like symptoms and disrupted navigation in Gnathonemus petersii, but a low dose of haloperidol did not normalize these symptoms.

Abstract

The present study aimed to examine a weakly electric fish Gnathonemus petersii (G. petersii) as a candidate model organism of glutamatergic theory of schizophrenia. The idea of G. petersii elevating the modeling of schizophrenia symptoms is based on the fish's electrolocation and electrocommunication abilities. Fish were exposed to the NMDA antagonist ketamine in two distinct series differing in the dose of ketamine. The main finding revealed ketamine-induced disruption of the relationship between electric signaling and behavior indicating impairment of fish navigation. Moreover, lower doses of ketamine significantly increased locomotion and erratic movement and higher doses of ketamine reduced the number of electric organ discharges indicating successful induction of positive schizophrenia-like symptoms and disruption of fish navigation. Additionally, a low dose of haloperidol was used to test the normalization of the positive symptoms to suggest a predictive validity of the model. However, although successfully induced, positive symptoms were not normalized using the low dose of haloperidol; hence, more doses of the typical antipsychotic haloperidol and probably also of a representative of atypical antipsychotic drugs need to be examined to confirm the predictive validity of the model.

Comparable studies

Other experimental studies on ketamine, most cited first.

Study Year Design Participants
Ketamine activates psychosis and alters limbic blood flow in schizophrenia Schizophrenic individuals 1995 Experimental study
The spectral exponent of the resting EEG indexes the presence of consciousness during unresponsiveness induced by propofol, xenon, and ketamine Healthy participants 2019 Controlled experimental study n = 15
Ketamine Increases Human Motor Cortex Excitability to Transcranial Magnetic Stimulation Normal human subjects 2003 Experimental study n = 7
Evidence that Subanesthetic Doses of Ketamine Cause Sustained Disruptions of NMDA and AMPA-Mediated Frontoparietal Connectivity in Humans Human participants 2015 Experimental study
S(+)-ketamine Effect on Experimental Pain and Cardiac Output Healthy adult volunteers (10 men and 10 women) 2009 Pharmacokinetic-pharmacodynamic modeling study in healthy volunteers n = 20

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