Effect of ketamine on exploratory behaviour in BALB/C and C57BL/6 mice

Akıllıoğlu, Kübra; Melik, Emine Babar; Melik, Enver; Boga, Ayper

doi:10.1016/j.pbb.2011.10.014

Cited by 23 publications

(27 citation statements)

References 37 publications

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“…Examining these mice in the open field test (OFT), we noted that changes in despair-like behavior in 2BΔCtx animals could not be accounted for by increased locomotor activity. Specifically, although total baseline locomotor activity is strongly increased in these 2BΔCtx animals, ketamine injection at this age caused a significant suppression of locomotion in both control and 2BΔCtx animals, indicating a dissociation of acute NMDAR suppression from locomotor activity, and consistent with previous data ( Figure 2D ) ( Akillioglu et al, 2012 ). At this same time point immobility scores actually decreased ( Figure 2B ).…”

Section: Resultssupporting

confidence: 91%

GluN2B-containing NMDA receptors regulate depression-like behavior and are critical for the rapid antidepressant actions of ketamine

Miller

Yang

Wang

et al. 2014

eLife

295

220

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A single, low dose of the NMDA receptor antagonist ketamine produces rapid antidepressant actions in treatment-resistant depressed patients. Understanding the cellular mechanisms underlying this will lead to new therapies for treating major depression. NMDARs are heteromultimeric complexes formed through association of two GluN1 and two GluN2 subunits. We show that in vivo deletion of GluN2B, only from principal cortical neurons, mimics and occludes ketamine's actions on depression-like behavior and excitatory synaptic transmission. Furthermore, ketamine-induced increases in mTOR activation and synaptic protein synthesis were mimicked and occluded in 2BΔCtx mice. We show here that cortical GluN2B-containing NMDARs are uniquely activated by ambient glutamate to regulate levels of excitatory synaptic transmission. Together these data predict a novel cellular mechanism that explains ketamine's rapid antidepressant actions. In this model, basal glutamatergic neurotransmission sensed by cortical GluN2B-containing NMDARs regulates excitatory synaptic strength in PFC determining basal levels of depression-like behavior.DOI: http://dx.doi.org/10.7554/eLife.03581.001

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Section: Resultssupporting

confidence: 91%

GluN2B-containing NMDA receptors regulate depression-like behavior and are critical for the rapid antidepressant actions of ketamine

Miller

Yang

Wang

et al. 2014

eLife

295

220

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“…We found a significant effect of strain [F(2,65)=4.42; p=0.016], with no effect of treatment [F(2,65)=2.37; p=0.13] and no interaction [F(2,65)=0.02; p=0.98]. Inter-strain comparisons indicated that Balb mice showed increased anxiety-like behaviour as compared to Bl6J (p=0.007), in agreement with previous data [43, 44]. Balb mice were also more anxious than Bl6N (p=0.02), while Bl6J and Bl6N strains did not differ (p=0.70), as already reported [45].…”

Section: Resultssupporting

confidence: 89%

A history of chronic morphine exposure during adolescence increases despair-like behaviour and strain-dependently promotes sociability in abstinent adult mice

Lutz

Reiss

Ouagazzal

et al. 2013

Behavioural Brain Research

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A crucial issue in treating opiate addiction, a chronic relapsing disorder, is to maintain a drug-free abstinent state. Prolonged abstinence associates with mood disorders, strongly contributing to relapse. In particular, substance use disorders occurring during adolescence predispose to depression later in adulthood. Using our established mouse model of opiate abstinence, we characterized emotional consequences into adulthood of morphine exposure during adolescence. Our results indicate that morphine treatment in adolescent mice has no effect on anxiety-like behaviours in adult mice, after abstinence. In contrast, morphine treatment during adolescence increases behavioural despair in adult mice. We also show that morphine exposure strain-dependently enhances sociability in adult mice. Additional research will be required to understand where and how morphine acts during brain maturation to affect emotional and social behaviours into adulthood.

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“…Moreover, we did not observe significant differences after acute ketamine administration, whether with single or multiple administration. The results of previous studies investigating the anxiety-related acute effects of ketamine were completely different, with reports of anxiolytic (Imre et al, 2006; Engin et al, 2009), anxiogenic (da Silva et al, 2010; Akillioglu et al, 2012), and null (Sobota et al, 2015) results. Some of the conclusions were inconsistent with our results.…”

Section: Discussionmentioning

confidence: 59%

“…We used the open field test to evaluate anxiety-like response after ketamine administration, as previously described (Akillioglu et al, 2012). The open field apparatus was a four-walled black plastic box that measured 40 cm × 40 cm × 30 cm (length/width/height) with a white bottom and no top.…”

Section: Methodsmentioning

confidence: 99%

Effects of Ketamine on Levels of Inflammatory Cytokines IL-6, IL-1β, and TNF-α in the Hippocampus of Mice Following Acute or Chronic Administration

Shen

Wen

et al. 2017

Front. Pharmacol.

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Ketamine is an injectable anesthetic and recreational drug of abuse commonly used worldwide. Many experimental studies have shown that ketamine can impair cognitive function and induce psychotic states. Neuroinflammation has been suggested to play an important role in neurodegeneration. Meanwhile, ketamine has been shown to modulate the levels of inflammatory cytokines. We hypothesized that the effects of ketamine on the central nervous system are associated with inflammatory cytokines. Therefore, we set out to establish acute and chronic ketamine administration models in C57BL/6 mice, to evaluate spatial recognition memory and emotional response, to analyze the changes in the levels of the inflammatory cytokines interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in the mouse hippocampus, employing behavioral tests, Western blot, quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and immunohistochemistry. Our results showed that ketamine at the dose of 60 mg/kg induced spatial recognition memory deficit and reduced anxiety-like behaviors in mice after chronic administration. Moreover, we found that ketamine increased the hippocampal levels of IL-6 and IL-1β after single, multiple and long-term administration in a dose-dependent manner. However, the expression level of TNF-α differed in the mouse hippocampus under different conditions. Single administration of ketamine increased the level of TNF-α, whereas multiple and long-term administration decreased it significantly. We considered that TNF-α expression could be controlled by a bi-directional regulatory pathway, which was associated with the dose and duration of ketamine administration. Our results suggest that the alterations in the levels of inflammatory cytokines IL-6, IL-1β, and TNF-α may be involved in the neurotoxicity of ketamine.

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Effect of ketamine on exploratory behaviour in BALB/C and C57BL/6 mice

Cited by 23 publications

References 37 publications

GluN2B-containing NMDA receptors regulate depression-like behavior and are critical for the rapid antidepressant actions of ketamine

GluN2B-containing NMDA receptors regulate depression-like behavior and are critical for the rapid antidepressant actions of ketamine

A history of chronic morphine exposure during adolescence increases despair-like behaviour and strain-dependently promotes sociability in abstinent adult mice

Effects of Ketamine on Levels of Inflammatory Cytokines IL-6, IL-1β, and TNF-α in the Hippocampus of Mice Following Acute or Chronic Administration

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