Quetiapine and repetitive transcranial magnetic stimulation ameliorate depression-like behaviors and up-regulate the proliferation of hippocampal-derived neural stem cells in a rat model of depression: The involvement of the BDNF/ERK signal pathway

Chen, Yi-huan; Zhang, Ruiguo; Xue, Fen; Wang, Huaning; Chen, Yun-chun; Hu, Guangtao; Ye, Peng; Peng, Zheng-wu; Tan, Qingrong

doi:10.1016/j.pbb.2015.07.005

Cited by 43 publications

(32 citation statements)

References 55 publications

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“…Recently, high-frequency rTMS at 20 Hz has been reported to stimulate the expression of BDNF in several brain regions in rats, including the hippocampal CA1 and CA3 subfields [14]. It has also been demonstrated that rTMS promotes the proliferation and increases the expression of pERK1/2 and BDNF in hippocampal-derived NSC [30]. Consistent with this, we found that both 20 Hz rTMS and iTBS significantly increased protein expression of BDNF and phosphorylated-TrkB, in parallel with enhanced levels of neurogenesis in the ipsilateral SVZ and peri-infarct striatum.…”

Section: Discussionmentioning

confidence: 99%

High-Frequency Repetitive Transcranial Magnetic Stimulation (rTMS) Improves Functional Recovery by Enhancing Neurogenesis and Activating BDNF/TrkB Signaling in Ischemic Rats

Luo

Zheng

Zhang

et al. 2017

IJMS

108

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Repetitive transcranial magnetic stimulation (rTMS) has rapidly become an attractive therapeutic approach for stroke. However, the mechanisms underlying this remain elusive. This study aimed to investigate whether high-frequency rTMS improves functional recovery mediated by enhanced neurogenesis and activation of brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) pathway and to compare the effect of conventional 20 Hz rTMS and intermittent theta burst stimulation (iTBS) on ischemic rats. Rats after rTMS were sacrificed seven and 14 days after middle cerebral artery occlusion (MCAO), following evaluation of neurological function. Neurogenesis was measured using specific markers: Ki67, Nestin, doublecortin (DCX), NeuN and glial fibrillary acidic protein (GFAP), and the expression levels of BDNF were visualized by Western blotting and RT-PCR analysis. Both high-frequency rTMS methods significantly improved neurological function and reduced infarct volume. Moreover, 20 Hz rTMS and iTBS significantly promoted neurogenesis, shown by an increase of Ki67/DCX, Ki67/Nestin, and Ki67/NeuN-positive cells in the peri-infarct striatum. These beneficial effects were accompanied by elevated protein levels of BDNF and phosphorylated-TrkB. In conclusion, high-frequency rTMS improves functional recovery possibly by enhancing neurogenesis and activating BDNF/TrkB signaling pathway and conventional 20 Hz rTMS is better than iTBS at enhancing neurogenesis in ischemic rats.

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Section: Discussionmentioning

confidence: 99%

High-Frequency Repetitive Transcranial Magnetic Stimulation (rTMS) Improves Functional Recovery by Enhancing Neurogenesis and Activating BDNF/TrkB Signaling in Ischemic Rats

Luo

Zheng

Zhang

et al. 2017

IJMS

108

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“…This is also the case for haloperidol which has similar affinity for S1R and D 2 R, because reduced haloperidol retains high affinity for S1R, has drastically reduced affinity for D 2 R, and it lacks the D 2 R-mediated antipsychotic activity and side effects of the parent compound haloperidol (Ulrich et al, 1999). Atypical antipsychotic drugs like clozapine, olanzapine, quetiapine, and aripiprazole have been reported to increase BDNF mRNA and/or protein levels in vivo (Chen et al, 2015b; Dong et al, 2016; Fumagalli et al, 2003; Murphy et al, 2014; Park et al, 2006; Seo et al, 2015; Shioda et al, 2015). Though in the case of these atypical antipsychotic drugs, the effects on BDNF are likely not mediated via the S1R, since, for example, clozapine has essentially no affinity for the S1R (Lee et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Activation of the sigma-1 receptor by haloperidol metabolites facilitates brain-derived neurotrophic factor secretion from human astroglia

Dalwadi

Kim

Schetz

2017

Neurochemistry International

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Glial cells play a critical role in neuronal support which includes the production and release of the neurotrophin brain-derived neurotrophic factor (BDNF). Activation of the sigma-1 receptor (S1R) has been shown to attenuate inflammatory stress-mediated brain injuries, and there is emerging evidence that this may involve a BDNF-dependent mechanism. In this report we studied S1R-mediated BDNF release from human astrocytic glial cells. Astrocytes express the S1R, which mediates BDNF release when stimulated with the prototypical S1R agonists 4-PPBP and (+)-SKF10047. This effect could be antagonized by a selective concentration of the S1R antagonist BD1063. Haloperidol is known to have high affinity interactions with the S1R, yet it was unable to facilitate BDNF release. Remarkably, however, two metabolites of haloperidol, haloperidol I and haloperidol II (reduced haloperidol), were discovered to facilitate BDNF secretion and this effect was antagonized by BD1063. Neither 4-PPBP, nor either of the haloperidol metabolites affected the level of BDNF mRNA as assessed by qPCR. These results demonstrate for the first time that haloperidol metabolites I and II facilitate the secretion of BDNF from astrocytes by acting as functionally selective S1R agonists.

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“…While to our knowledge, there is still no experimental study on direct magnetic stimulation of the hippocampus up to now. Evidence from many studies has revealed that BDNF is involved in the survival and proliferation of new neurons [47, 48] and increasing of BDNF level is closely associated with the depression improvement [32, 36]. We supposed that the SPIO+RMF may take effect by affecting hippocampal neurogenesis or affecting BDNF signaling pathway.…”

Section: Discussionmentioning

confidence: 98%

“…Moreover, numerous experimental compounds and drugs are suggested to improve depressive-like behaviors by altering the protein expression, or the signaling pathway of BDNF at a deeper level [33, 34, 35]. Corresponding to compounds and drugs, BDNF was reported to be correlated with the antidepressive effects of rTMS [36]. A review calimed that BDNF is the most promising predictor of MDD victims’ respondence to TMS[37].…”

Section: Methodsmentioning

confidence: 99%

Precise implantation of super-paramagnetic iron oxide (SPIO) nanoparticles in hippocampus with external rotating magnetic field (RMF) produces rapid antidepressent effects in mice

Chi

Cai

Mengqin

et al. 2019

Preprint

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BackgroundTMS is an effective anti-depression method commonly used in clinical practice, but it also faces the problems of low spatial resolution, treatment parameters to be optimized and limitation in mechanism research.ObjectiveTo develop a precise magnetic stimulation anti-depression method for the scientific research of magnetic stimulation, especially the mechanism research in animal experiments.MethodsThe cytotoxicity test was conducted in advance to ensure the security of intervention from SPIO nanoparticles and RMF. In animal experiments, 300nl SPIO solution was injected into the right hippocampus of the CUMS model mice, and then treated experimental group mice with rotating magnetic field for five days. The Sucrose Preference Test (SPT), the Forced Swim Test (FST) and BDNF expression levels were used to evaluate the antidepressant effect of this method.ResultsNo significant decrease of cell viability was observed when the iron concentration is between 52.2µg/ml and 208.8µg/ml. And the application of RMF with a certain frequency was considered to be safe in the cytotoxicity test. When treated with SPIO+RMF, the sucrose preference of SPIO+RMF group mice increased markedly (n=9, p<0.01 vs. CUMS), the FST immobile time reduced (n=8, P<0.05 vs. CUMS) and the BDNF level in the hippocampus was significantly up-regulated (n=5, P<0.01 vs. CUMS). However, merely SPIO intervention failed to be effective.Conclusionswhen intervened with external rotating magnetic field, the SPIO nanoparticles injected into the right hippocampus could produce rapid antidepressent effects in mice.

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Quetiapine and repetitive transcranial magnetic stimulation ameliorate depression-like behaviors and up-regulate the proliferation of hippocampal-derived neural stem cells in a rat model of depression: The involvement of the BDNF/ERK signal pathway

Cited by 43 publications

References 55 publications

High-Frequency Repetitive Transcranial Magnetic Stimulation (rTMS) Improves Functional Recovery by Enhancing Neurogenesis and Activating BDNF/TrkB Signaling in Ischemic Rats

High-Frequency Repetitive Transcranial Magnetic Stimulation (rTMS) Improves Functional Recovery by Enhancing Neurogenesis and Activating BDNF/TrkB Signaling in Ischemic Rats

Activation of the sigma-1 receptor by haloperidol metabolites facilitates brain-derived neurotrophic factor secretion from human astroglia

Precise implantation of super-paramagnetic iron oxide (SPIO) nanoparticles in hippocampus with external rotating magnetic field (RMF) produces rapid antidepressent effects in mice

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