Neurochemical and molecular characterization of ketamine-induced experimental psychosis model in mice

Chatterjee, Manavi; Verma, Rajkumar; Ganguly, Shantanu; Palit, Gautam

doi:10.1016/j.neuropharm.2012.05.041

Cited by 125 publications

(97 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It´s important to consider that in our work, the persistence of ketamine´s effect was evaluated swimming. Futhermore, in their first studies Noda et al (1995) showed the persistence of phencyclidine proimmobility effect using the same experimental design as our, and similar results were also described for MK-801 (Langen et al 2012) and even for the high ketamine dose (Chatterjee et al 2012).…”

Section: Immobility Behavior For Modeling Schizophrenias 1663supporting

confidence: 82%

Is Forced Swimming Immobility a Good Endpoint for Modeling Negative Symptoms of Schizophrenia? - Study of Sub-Anesthetic Ketamine Repeated Administration Effects

Neves

Borsoi

Antonio

et al. 2017

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

Immobility time in the forced swimming has been described as analogous to emotional blunting or apathy and has been used for characterizing schizophrenia animal models. Several clinical studies support the use of NMDA receptor antagonists to model schizophrenia in rodents. Some works describe the effects of ketamine on immobility behavior but there is variability in the experimental design used leading to controversial results. In this study, we evaluated the effects of repeated administration of ketamine subanesthetic doses in forced swimming, locomotion in response to novelty and novel object recognition, aiming a broader evaluation of the usefulness of this experimental approach for modeling schizophrenia in mice. Ketamine (30 mg/kg/day i.p. for 14 days) induced a not persistent decrease in immobility time, detected 24h but not 72h after treatment. This same administration protocol induced a deficit in novel object recognition. No change was observed in mice locomotion. Our results confirm that repeated administration of sub-anesthetic doses of ketamine is useful in modeling schizophrenia-related behavioral changes in mice. However, the immobility time during forced swimming does not seem to be a good endpoint to evaluate the modeling of negative symptoms in NMDAR antagonist animal models of schizophrenia.

show abstract

Section: Immobility Behavior For Modeling Schizophrenias 1663supporting

confidence: 82%

Is Forced Swimming Immobility a Good Endpoint for Modeling Negative Symptoms of Schizophrenia? - Study of Sub-Anesthetic Ketamine Repeated Administration Effects

Neves

Borsoi

Antonio

et al. 2017

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

show abstract

“…This disinhibitory action has been reported to increase the neuronal activity and excessive dopamine release in the limbic striatal regions. Our investigations revealed an over activity of the dopaminergic pathway in response to ketamine administration (Chatterjee et al, 2012c). Moreover, the locomotor deficits induced by ketamine were restored significantly following exposure to BM likely due to partial restoration of striatal DA levels.…”

Section: Discussionmentioning

confidence: 54%

Antipsychotic activity of standardizedBacopaextract against ketamine-induced experimental psychosis in mice: Evidence for the involvement of dopaminergic, serotonergic, and cholinergic systems

Chatterjee

Verma

Kumari

et al. 2015

Pharmaceutical Biology

Self Cite

View full text Add to dashboard Cite

(2015) Antipsychotic activity of standardized Bacopa extract against ketamine-induced experimental psychosis in mice: Evidence for the involvement of dopaminergic, serotonergic, and cholinergic systems, Pharmaceutical Biology, 53:12, 1850-1860, DOI: 10.3109/13880209.2014 (40, 80, and 120 mg/kg, p.o.) were given to the mice 1 h prior to ketamine administration and tested for positive symptoms and cognitive deficits. A chronic ketamine treatment regimen was used to study the effect of BM on negative symptoms such as immobility enhancement. Each mouse was used once for the behavioral studies.Results: BM reduced ketamine-induced hyperactivity with an EC 50 value of 76.60 mg/kg. The 80 mg/kg dose was used for all other behavior analysis. Pretreatment with BM at 80 mg/kg showed two-fold increases in transfer latency time (TLT) in passive avoidance task. Chronic BM pretreatment (80 mg/kg p.o. daily Â 10 d) ameliorated the ketamine-induced enhanced immobility effect by 21% in the forced swim test. BM treatment reversed ketamine-induced increase in monoamine oxidase activity in both cortex and striatum and normalized the acetylcholinesterase activity and the glutamate levels in the hippocampus. Discussion and conclusion: Overall our findings suggest that BM possesses antipsychotic properties which might be due to its modulatory action on dopamine, serotonin, and glutamate neurotransmission.

show abstract

“…It is important to note that biochemical data have shown that neurotransmitter like dopamine is implicated in central nervous system excitation [16]. Therefore, the decrease in NIR in this study by DOX is suggestive of possible interference with central dopaminergic neurotransmission and tranquilizing effect.…”

Section: Discussionmentioning

confidence: 60%

“…Because the systemic administration of dopamine antagonists counteracts the hyperlocomotion induced by the administration of NMDA receptor antagonist [37], it is therefore; suggestive that dopamine neurotransmission is involved in the motor activating effects of ketamine-induced hyperlocomotion [16]. .…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, recent findings from preclinical studies suggest possible beneficial effects of minocycline as adjunctive therapy for the treatment of negative and cognitive symptoms of schizophrenia [13] [14]. In this context, the therapeutic properties of doxycycline relative to that of minocycline, suggests that it may also have clinical application in schizophrenia symptomology, most especially against the negative and cognitive symptoms of the disease [15] [16]. Therefore, this study was designed to evaluate the antipsychotic property of doxycycline by specifically investigating its effects on: 1) positive schizophrenia-like behavior, 2) negative schizophrenia-like behavior, 3) cognitive schizophrenia-like behavior and 4) biomarkers of oxidative stress in mouse brain.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Doxycycline Ameliorates Schizophrenia-Like Behaviors in Experimental Models in Mice by Targeting Underlying Oxidative Stress

Ben-Azu¹,

Omogbiya²,

Aderibigbe³

et al. 2016

JBBS

View full text Add to dashboard Cite

Current evidences support the inhibition of oxidative and inflammatory signaling mechanisms in the treatment of schizophrenia; as cure for this disease still remains limited. Doxycycline is a tetracycline antibiotic (a minocycline congener) with strong antioxidant and anti-inflammatory properties, and better pharmacokinetic profiles. Preclinical evidence indicates that minocycline possesses antipsychotic properties. This present study was designed to evaluate the effect of doxycycline on schizophrenialike behaviors, as well as biomarkers of oxidative stress in mice brains. Noveltyinduced rearing (NIR) behavior was used to evaluate the tranquilizing effect of doxycycline (25 -200 mg/kg). The acute antipsychotic effects of doxycycline were assessed using apomorphine-induced stereotypy, ketamine-induced stereotypy, hyperlocomotion and enhanced immobility in forced swim test (FST). Catalepsy test was also employed to evaluate the extrapyramidal adverse effect of doxycycline in mice. The chronic antipsychotic effect of doxycycline was evaluated following oral administration of doxycycline in combination with ketamine (100 mg/kg) intraperitoneally for 10 days. Twenty four hours after the last administration, positive (locomotor activity), cognitive (Y-maze) and negative (FST) symptoms were assessed. Thereafter, levels of biomarkers of oxidative stress were evaluated in mice brains. Doxycycline significantly (P < 0.05) decreased NIR, inhibited stereotypy induced by apomorphine and ketamine. Additionally, doxycycline significantly (P < 0.05) prevented ketamineinduced hyperlocomotion, cognitive deficit and reduced enhanced-immobility by ketamine in mice. Furthermore, doxycycline decreased malondialdehyde concentrations in a dose-related manner. Moreover, doxycycline significantly (P < 0.05) prevented the decrease in glutathione, and increased activities of superoxide dismutase and catalase in brain tissues. The results from this study suggest that doxycycline 540ameliorated schizophrenic-like behaviors via mechanisms related to attenuation of oxidative stress in mouse brain.

show abstract

Neurochemical and molecular characterization of ketamine-induced experimental psychosis model in mice

Cited by 125 publications

References 40 publications

Is Forced Swimming Immobility a Good Endpoint for Modeling Negative Symptoms of Schizophrenia? - Study of Sub-Anesthetic Ketamine Repeated Administration Effects

Is Forced Swimming Immobility a Good Endpoint for Modeling Negative Symptoms of Schizophrenia? - Study of Sub-Anesthetic Ketamine Repeated Administration Effects

Antipsychotic activity of standardizedBacopaextract against ketamine-induced experimental psychosis in mice: Evidence for the involvement of dopaminergic, serotonergic, and cholinergic systems

Doxycycline Ameliorates Schizophrenia-Like Behaviors in Experimental Models in Mice by Targeting Underlying Oxidative Stress

Contact Info

Product

Resources

About