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

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023752%3A_____%2F23%3A43921056" target="_blank" >RIV/00023752:_____/23:43921056 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216224:90249/23:00133574 RIV/00216208:11310/23:10457601 RIV/00216208:11120/23:43925212

Výsledek na webu

<a href="https://onlinelibrary.wiley.com/doi/10.1002/jnr.25186" target="_blank" >https://onlinelibrary.wiley.com/doi/10.1002/jnr.25186</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/jnr.25186" target="_blank" >10.1002/jnr.25186</a>

Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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&apos;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.

Název v anglickém jazyce

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

Popis výsledku anglicky

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&apos;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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2023

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Neuroscience Research

ISSN

0360-4012

e-ISSN

1097-4547

Svazek periodika

101

Číslo periodika v rámci svazku

7

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

9

Strana od-do

1098-1106

Kód UT WoS článku

000943024600001

EID výsledku v databázi Scopus

2-s2.0-85150229324