Common cellular and molecular mechanisms and interactions between microglial activation and aberrant neuroplasticity in depression

Guo, Xiaoyun; Rao, Yu; Mao, Ruizhi; Cui, Lvchun; Fang, Yiru

doi:10.1016/j.neuropharm.2020.108336

Cited by 22 publications

(18 citation statements)

References 145 publications

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Section: Discussionsupporting

confidence: 92%

“…After SCI, a large number of microglia are stimulated and change their morphology and function, mainly those related to the M1 phenotype. Similarly, LPS induces the polarization of microglia toward the M1 phenotype and increased the secretion of proinflammatory factors 29. These phenomena are consistent with what we observed in this study.Numerous studies have shown that inhibiting M1 polarization while inducing the transformation of microglia from the M1 phenotype to the M2 phenotype is more conducive to inhibiting neuroinflammation than simply inhibiting M1 37.…”

supporting

confidence: 92%

“…SCI is a serious disabling disease and inflammation is the most critical pathologic change that occurs during the secondary injury phase 27 . Previous reports have proven that microglia/macrophages can be divided into two main subgroups, namely M1 (proinflammatory) microglia/macrophages and M2 (anti‐inflammatory) microglia/macrophages 28,29 . Therefore, inflammation may be ameliorated by promoting the transformation of M1 into M2 30 .…”

Section: Discussionmentioning

confidence: 99%

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Atractylenolide III ameliorates spinal cord injury in rats by modulating microglial/macrophage polarization

et al. 2022

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Background Inflammatory reactions induced by spinal cord injury (SCI) are essential for recovery after SCI. Atractylenolide III (ATL‐III) is a natural monomeric herbal bioactive compound that is mainly derived in Atractylodes macrocephala Koidz and has anti‐inflammatory and neuroprotective effects. Objective Here, we speculated that ATL‐III may ameliorate SCI by modulating microglial/macrophage polarization. In the present research, we focused on investigating the role of ATL‐III on SCI in rats and explored the potential mechanism. Methods The protective and anti‐inflammatory effects of ATL‐III on neuronal cells were examined in a rat SCI model and lipopolysaccharide (LPS)‐stimulated BV2 microglial line. The spinal cord lesion area, myelin integrity, and surviving neurons were assessed by specific staining. Locomotor function was evaluated by the Basso, Beattie, and Bresnahan (BBB) scale, grid walk test, and footprint test. The activation and polarization of microglia/macrophages were assessed by immunohistofluorescence and flow cytometry. The expression of corresponding inflammatory factors from M1/M2 and the activation of relevant signaling pathways were assessed by Western blotting. Results ATL‐III effectively improved histological and functional recovery in SCI rats. Furthermore, ATL‐III promoted the transformation of M1 into M2 and attenuated the activation of microglia/macrophages, further suppressing the expression of corresponding inflammatory mediators. This effect may be partly mediated by inhibition of neuroinflammation through the NF‐κB, JNK MAPK, p38 MAPK, and Akt pathways. Conclusion This study reveals a novel effect of ATL‐III in the regulation of microglial/macrophage polarization and provides initial evidence that ATL‐III has potential therapeutic benefits in SCI rats.

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Section: Discussionsupporting

confidence: 92%

supporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

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Atractylenolide III ameliorates spinal cord injury in rats by modulating microglial/macrophage polarization

et al. 2022

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“…Neuroplasticity is closely associated with the development of depression. MiRNAs are involved in this process and play important roles [18] (Figure 1). The up or downregulation of miRNA expression levels leads to impaired neuroplasticity and is involved in the pathogenesis of depression.…”

Section: Mirnas and Neuroplasticity In Depressionmentioning

confidence: 99%

A New Player in Depression: MiRNAs as Modulators of Altered Synaptic Plasticity

Gao

Zhang

Wang

et al. 2022

IJMS

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Depression is a psychiatric disorder that presents with a persistent depressed mood as the main clinical feature and is accompanied by cognitive impairment. Changes in neuroplasticity and neurogenesis greatly affect depression. Without genetic changes, epigenetic mechanisms have been shown to function by regulating gene expression during the body’s adaptation to stress. Studies in recent years have shown that as important regulatory factors in epigenetic mechanisms, microRNAs (miRNAs) play important roles in the development and progression of depression through the regulation of protein expression. Herein, we review the mechanisms of miRNA-mediated neuroplasticity in depression and discus synaptic structural plasticity, synaptic functional plasticity, and neurogenesis. Furthermore, we found that miRNAs regulate neuroplasticity through several signalling pathways to affect cognitive functions. However, these pathways do not work independently. Therefore, we try to identify synergistic correlations between miRNAs and multiple signalling pathways to broaden the potential pathogenesis of depression. In addition, in the future, dual-function miRNAs (protection/injury) are promising candidate biomarkers for the diagnosis of depression, and their regulated genes can potentially be used as target genes for the treatment of depression.

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“…In the amygdala, chronic stress leads to decreased glutamate release, impaired or enhanced LTP, dendritic hypertrophy, increased dendritic spines, and anxiety (Reznikov et al, 2011). Guo et al (2020) have suggested that the negative impact of stress may be due to activation of the microglial cells, which trigger neuroinflammation, affecting both intracellular and extracellular signaling pathways. Furthermore, stress is also known to increase LTD while decreasing LTP (Wong et al, 2007;Reznikov et al, 2011).…”

Section: Neuroplasticitymentioning

confidence: 99%

Glutamate: The Master Neurotransmitter and Its Implications in Chronic Stress and Mood Disorders

Pal

2021

Front. Hum. Neurosci.

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This brief review article makes the argument that glutamate is deserving of its newfound attention within the neuroscience literature and that many directions of important research have yet to be explored. Glutamate is an excitatory neurotransmitter with several types of receptors found throughout the central nervous system, and its metabolism is important to maintaining optimal levels within the extracellular space. As such, it is important to memory, cognition, and mood regulation. The mechanisms by which chronic stress affect the glutamatergic system and neuroplasticity are outlined. Several implications for potential pharmacologic and non-pharmacologic interventions are discussed.

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Common cellular and molecular mechanisms and interactions between microglial activation and aberrant neuroplasticity in depression

Cited by 22 publications

References 145 publications

Atractylenolide III ameliorates spinal cord injury in rats by modulating microglial/macrophage polarization

Atractylenolide III ameliorates spinal cord injury in rats by modulating microglial/macrophage polarization

A New Player in Depression: MiRNAs as Modulators of Altered Synaptic Plasticity

Glutamate: The Master Neurotransmitter and Its Implications in Chronic Stress and Mood Disorders

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