Ketamine improved depressive-like behaviors via hippocampal glucocorticoid receptor in chronic stress induced- susceptible mice

Wang, Wei; Liu, Le; Yang, Xiu Hong; Gao, Han; Tang, Qikai; Yin, Luo-Yue; Yin, Xiaoyu; Hao, Jing‐Ru; Geng, Deqin; Gao, Can

doi:10.1016/j.bbr.2019.01.057

Cited by 50 publications

(51 citation statements)

References 73 publications

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“…Recently, ketamine had been introduced as a potent antidepressant. A single subanesthetic dose of ketamine could produce rapid, profound, and long‐lasting antidepressant effect in animal studies and also in clinical trials 4,7 . Therefore, we conduct the study to examine whether if low‐dose ketamine could ameliorate stress‐induced disorders in mice and the role of brain‐derived neurotrophic factor (BDNF) in this animal model.…”

Section: Introductionmentioning

confidence: 99%

Does ketamine ameliorate the social stress‐related bladder dysfunction in mice?

Yang

Chang

2020

Neurourology and Urodynamics

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Aims The aim of this study is to investigate whether ketamine could relieve the social stress (SS)‐related bladder dysfunction in mice. Materials and Methods The FVB mice were randomly assigned to either undergo SS exposure for 60 minutes per day on seven consecutive days for 4 weeks (SS1) or control without SS (SS0). The SS0 were then allocated to single or no injection of ketamine (SS0K1 and SS0K0). In the group of SS1, the SS1 mice were allocated to receive single injection of saline (SS1K0), single dose (SS1K1) or five daily dose of (SS1K5) ketamine injection (25 mg/kg/day/ip) since day 22. In vivo cystometry and tissue bath wire myography were performed on day 29. Serum and urine level of brain‐derived neurotrophic factor (BDNF) were measured with enzyme‐linked immunosorbent assay. Results In mice without social stress exposure, ketamine administration did not significantly affect voiding frequency (P > .05). SS1K0, SS1K1, and SS1K5 had significantly lower voiding frequency than that of control (SS1K0) (each n = 15, P < .05). Ketamine administration reversed the trend of decreased voiding frequency in SS1 mice. Stressed mice had significant higher serum level of BDNF that reduced by short‐term ketamine. Stressed mice had detrusor overactivity and impaired detrusor contractility which were not reversed by short‐term ketamine. Conclusions Social stress leads to elevated serum BDNF, infrequent voiding, detrusor overactivity, and impaired contractility. Short‐term administration of ketamine may improve SS‐related infrequent voiding and elevated serum BDNF level. However, ketamine did not improve SS‐related bladder dysfunction on urodynamic and myography studies.

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Section: Introductionmentioning

confidence: 99%

Does ketamine ameliorate the social stress‐related bladder dysfunction in mice?

Yang

Chang

2020

Neurourology and Urodynamics

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“…Ketamine was recently reported to increase activity of the GR (Wang et al, 2019) and therefore it was surprising that we did not find any effects of ketamine on levels of GR or pGR in the PFC or Hippocampus. Furthermore, since it has been established that JNK phosphorylates (and thereby deactivates) the GR, we would expect that the increased pJNK in the PFC of ketamine-treated mice would have been associated with increases in pGR as well.…”

Section: Discussionmentioning

confidence: 50%

“…Likewise, ketamine has recently been reported to increase GR expression and activity in the hippocampus (Wang et al, 2019). Moreover, in the study by Wang et al (2019), ketamine's antidepressant-like effects were dependent upon its modulation of the GR.…”

Section: Introductionmentioning

confidence: 81%

“…Although ketamine did not alter corticosterone levels in any of our tests, it is possible that ketamine administration could theoretically modulate the spike in corticosterone caused by JNK inhibition through its own interaction with the GR. Indeed, ketamine has very recently been shown to improve depressive-like behaviors in chronically stressed mice, and that effect was associated with the rescue of both stress-induced GR reductions, and reductions in the nuclear translocation of the GR (Wang et al, 2019). In…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, JNK has been found to negatively regulate the GR, whose activation is associated with depression-related processes including neurogenesis, inhibition of inflammation, and HPA axis regulation (Munck, 2005;Davies et al, 2008;Kadmiel and Cidlowski, 2013). Likewise, ketamine has recently been reported to increase GR expression and activity in the hippocampus (Wang et al, 2019). Moreover, in the study by Wang et al (2019), ketamine's antidepressant-like effects were dependent upon its modulation of the GR.…”

Section: Introductionmentioning

confidence: 98%

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Novel Treatment Strategies for Major Depressive Disorder: Investigating Ketamine’s Antidepressant Effects and the Role of the c-Jun N-Terminal Kinase Pathway

Clarke¹

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Current first-line treatments for depression, namely monoamine-based drugs such as SSRIs, take weeks to show any clinical effects, and they are only effective in 60-70% of patients. There is therefore an urgent need to develop more rapid and efficacious treatments. Ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist often used as a dissociative anesthetic, has been found to have rapid (within hours) antidepressant effects, even in historically treatment-resistant patients. Nevertheless, ketamine has its own limitations, such as unwanted side effects and abuse potential. The overarching goal of this thesis was to gain a better understanding of the antidepressant mechanisms of ketamine. Dedication To my family, all of you. Only you know how long this road has really been, and your support has been absolutely paramount. Thank you. v Table of Contents Abstract…………………………………………………………………………………ii Acknowledgements…………………………………………………………………..iii Dedication……………………………………………………………………………...iv Table of Contents…………………………………………………………………......v List of Figures…………………………………………………………………….....viii List of Abbreviations………………………………………………………………..xi Preface………………………………………………………………………………...xiii Chapter 1. General Introduction…………………………………………………1 Chapter 2. Ketamine modulates pro-inflammatory cytokines, but not stressor-induced neurochemical changes……………………………………...27

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The Glutamatergic System in Treatment-Resistant Depression and Comparative Effectiveness of Ketamine and Esketamine: Role of Inflammation?

Halaris

Cook

2023

Advances in Experimental Medicine and Biology

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Ketamine improved depressive-like behaviors via hippocampal glucocorticoid receptor in chronic stress induced- susceptible mice

Cited by 50 publications

References 73 publications

Does ketamine ameliorate the social stress‐related bladder dysfunction in mice?

Does ketamine ameliorate the social stress‐related bladder dysfunction in mice?

Novel Treatment Strategies for Major Depressive Disorder: Investigating Ketamine’s Antidepressant Effects and the Role of the c-Jun N-Terminal Kinase Pathway

The Glutamatergic System in Treatment-Resistant Depression and Comparative Effectiveness of Ketamine and Esketamine: Role of Inflammation?

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