RESUMO
Spatial transcriptomics is an omics technology that realizes the determination of cell spatial location information on the basis of single cell RNA sequencing. This technology overcomes the problem of losing the spatial information of cells in the tissue during the single-cell isolation of single cell RNA sequencing. Spatial transcriptomics can provide both transcriptome information and spatial location information of research objects in tissues. Spatial transcriptomics plays an important role in the study of cell lineage generation, regulation mechanism and interaction between cells, and is an important development direction and hot spot of omics technology research. In recent years, spatial transcriptomics technology has developed rapidly, new detection methods have been continuously produced, and technical indicators such as detection sensitivity, resolution and detection throughput have been continuously improved. According to the different principles of obtaining spatial information, this paper classifies the commonly used spatial transcriptomics techniques, and summarizes the detection principles, representative technical methods and technical indicators. Then, the application of spatial transcriptomics technology in neuroscience is expounded from two aspects: differentiation of brain cell types and construction of cell layer maps, and analysis of characteristics of diseases and biomarker related to nervous systems. Finally, we summarize the current problems of spatial transcriptomics technology and give an outlook on its future development direction.
RESUMO
Radiotherapy-related pain is a common adverse reaction with a high incidence among cancer patients undergoing radiotherapy and remarkably reduces the quality of life. However, the mechanisms of ionizing radiation-induced pain are largely unknown. In this study, mice were treated with 20 Gy X-ray to establish ionizing radiation-induced pain model. X-ray evoked a prolonged mechanical, heat, and cold allodynia in mice. Transient receptor potential vanilloid 1 and transient receptor potential ankyrin 1 were significantly upregulated in lumbar dorsal root ganglion. The mechanical and heat allodynia could be transiently reverted by intrathecal injection of transient receptor potential vanilloid 1 antagonist capsazepine and transient receptor potential ankyrin 1 antagonist HC-030031. Additionally, the phosphorylated extracellular regulated protein kinases (ERK) and Jun NH2-terminal Kinase (JNK) in pain neural pathway were induced by X-ray treatment. Our findings indicated that activation of transient receptor potential ankyrin 1 and transient receptor potential vanilloid 1 is essential for the development of X-ray-induced allodynia. Furthermore, our findings suggest that targeting on transient receptor potential vanilloid 1 and transient receptor potential ankyrin 1 may be promising prevention strategies for X-ray-induced allodynia in clinical practice.
Assuntos
Temperatura Alta , Hiperalgesia/metabolismo , Ativação do Canal Iônico , Canal de Cátion TRPA1/metabolismo , Canais de Cátion TRPV/metabolismo , Animais , Comportamento Animal , Modelos Animais de Doenças , Gânglios Espinais/metabolismo , Gânglios Espinais/patologia , Gânglios Espinais/efeitos da radiação , Ativação do Canal Iônico/efeitos da radiação , Sistema de Sinalização das MAP Quinases/efeitos da radiação , Masculino , Camundongos Endogâmicos C57BL , Vias Neurais/efeitos da radiação , Estresse Oxidativo/efeitos da radiação , Dor/metabolismo , Dor/patologia , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Canal de Cátion TRPA1/antagonistas & inibidores , Canais de Cátion TRPV/antagonistas & inibidores , Fatores de Tempo , Raios XRESUMO
The present study was designed to examine the therapeutic effects of Botulinum neurotoxin A (BoNT/A) on depression-like behaviors in mice and to explore the potential mechanisms. These results revealed that a single facial injection of BoNT/A induced a rapid and prolonged improvement of depression-like behaviors in naïve and space-restriction-stressed (SRS) mice, reflected by a decreased duration of immobility in behavioral despair tests. BoNT/A significantly increased the 5-hydroxytryptamine (5-HT) levels in several brain regions, including the hippocampus and hypothalamus, in SRS mice. BoNT/A increased the expression of the N-methyl-D-aspartate receptor subunits NR1 and NR2B in the hippocampus, which were significantly decreased in SRS mice. Furthermore, BoNT/A significantly increased the expression of brain-derived neurotrophic factor (BDNF) in the hippocampus, hypothalamus, prefrontal cortex, and amygdala, which were decreased in SRS mice. Finally, BoNT/A transiently increased the levels of phosphorylated extracellular signal-regulated kinase (p-ERK) and cAMP-response element binding protein (p-CREB), which were suppressed in the hippocampus of SRS mice. Collectively, these results demonstrated that BoNT/A treatment has anti-depressant-like activity in mice, and this is associated with increased 5-HT levels and the activation of BDNF/ERK/CREB pathways in the hippocampus, supporting further investigation of BoNT/A therapy in depression.
RESUMO
In the original publication, Figure 4G was incorrectly published. The correct version of Figure 4G is presented in this correction. This correction does not affect the conclusions of the paper.
