The Experts below are selected from a list of 1548 Experts worldwide ranked by ideXlab platform

You Wan - One of the best experts on this subject based on the ideXlab platform.

  • Hypersensitivity of Prelimbic Cortex Neurons Contributes to Aggravated Nociceptive Responses in Rats With Experience of Chronic Inflammatory Pain.
    Frontiers in molecular neuroscience, 2018
    Co-Authors: Xiao-cen Fan, Feng-yu Liu, Shuang Cui, You Wan
    Abstract:

    Previous experience of Chronic Pain causes enhanced responses to upcoming noxious events in both humans and animals, but the underlying mechanisms remain unclear. In the present study, we found that rats with complete Freund's adjuvant (CFA)-induced Chronic Inflammatory Pain experience exhibited aggravated Pain responses to later formalin test. Enhanced neuronal activation upon formalin assaults and increased phosphorylated cAMP-response element binding protein (CREB) were observed in the prelimbic cortex (PL) of rats with Chronic Inflammatory Pain experience, and inhibiting PL neuronal activities reversed the aggravated Pain. Inflammatory Pain experience induced persistent p38 mitogen-activated protein kinase (MAPK; p38) but not extracellular regulated protein kinase (ERK) or c-Jun N-terminal kinase (JNK) hyperphosphorylation in the PL. Inhibiting the p38 phosphorylation in PL reversed the aggravated nociceptive responses to formalin test and down-regulated enhanced phosphorylated CREB in the PL. Chemogenetics identified PL-periaqueductal gray (PAG) but not PL-nucleus accumbens (NAc) as a key pathway in inducing the aggravated formalin Pain. Our results demonstrate that persistent hyperphosphorylation of p38 in the PL underlies aggravated nociceptive responses in rats with Chronic Inflammatory Pain experience.

  • The Frontal Area with Higher Frequency Response Is the Principal Feature of Laser-Evoked Potentials in Rats with Chronic Inflammatory Pain: A Parallel Factor Analysis Study.
    Frontiers in neurology, 2017
    Co-Authors: Jing Wang, Juan Wang, You Wan
    Abstract:

    Chronic Pain is a pathological developing course of Pain. In clinic, an objective indicator is needed for diagnosing and better controlling Chronic Pain. The abnormal neural responses in Chronic Pain are reflected by multiple event-related potentials (ERPs) in time, frequency and location domain respectively. However, multiple changes in ERPs are not applicable in clinic. So, the principal feature covered the most informative changes extracted from these three domains of ERP during the development of Chronic Pain is needed. In the present study, a parallel factor analysis (PARAFAC) method was employed to extract time-frequency-channel features of laser evoked potential (LEP) simultaneously from rats with Chronic Inflammatory Pain. Results showed that the main feature of LEP in channel domain locates in the frontal brain region in rats with Chronic Inflammatory Pain while in the parietal brain region in control rats. In the frequency domain, the main frequency of LEP was significantly higher in Chronic Inflammatory Pain rats than that in control rats. These findings indicate that the frontal region with higher frequency response to nociceptive information is the principal feature in the Chronic Pain state. Our study provided not only a principal feature of LEP but also a promising strategy for Chronic Pain which is potential for clinic application.

  • Adult hippocampal neurogenesis along the dorsoventral axis contributes differentially to environmental enrichment combined with voluntary exercise in alleviating Chronic Inflammatory Pain in mice
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017
    Co-Authors: Jie Zheng, Fei-fei Liao, Feng-yu Liu, Jie Cai, Shuang Cui, Ying-ying Jiang, You Wan
    Abstract:

    Cognitive behavioral therapy, such as environmental enrichment combined with voluntary exercise (EE-VEx), is under active investigation as an adjunct to pharmaceutical treatment for Chronic Pain. However, the effectiveness and underlying mechanisms of EE-VEx remain unclear. In mice with intraplantar injection of complete Freund's adjuvant, our results revealed that EE-VEx alleviated perceptual, affective, and cognitive dimensions of Chronic Inflammatory Pain. These effects of EE-VEx on Chronic Pain were contingent on the occurrence of adult neurogenesis in the dentate gyrus in a functionally dissociated manner along the dorsoventral axis: neurogenesis in the ventral dentate gyrus participated in alleviating perceptual and affective components of Chronic Pain by EE-VEx, whereas neurogenesis in the dorsal dentate gyrus was involved in EE-VEx's cognitive-enhancing effects. Chronic Inflammatory Pain was accompanied by decreased levels of brain-derived neurotrophic factor (BDNF) in the dentate gyrus, which were reversed by EE-VEx. Overexpression of BDNF in the dentate gyrus mimicked the effects of EE-VEx. Our results demonstrate distinct contribution of adult hippocampal neurogenesis along the dorsoventral axis to EE-VEx's beneficial effects on different dimensions of Chronic Pain.SIGNIFICANCE STATEMENT Environmental enrichment combined with voluntary exercise (EE-VEx) is under active investigation as an adjunct to pharmaceutical treatment for Chronic Pain, but its effectiveness and underlying mechanisms remain unclear. In a mouse model of Inflammatory Pain, the present study demonstrates that the beneficial effects of EE-VEx on Chronic Pain depend on adult neurogenesis with a dorsoventral dissociation along the hippocampal axis. Adult neurogenesis in the ventral dentate gyrus participates in alleviating perceptual and affective components of Chronic Pain by EE-VEx, whereas that in the dorsal pole is involved in EE-VEx's cognitive-enhancing effects in Chronic Pain.

  • Reduced GABAergic transmission in the ventrobasal thalamus contributes to thermal hyperalgesia in Chronic Inflammatory Pain.
    Scientific reports, 2017
    Co-Authors: Chan Zhang, Rongxiang Chen, Fei-fei Liao, Jie Wang, Yu Zhang, Feng-yu Liu, Jie Cai, You Wan
    Abstract:

    The ventrobasal (VB) thalamus is innervated by GABAergic afferents from the thalamic reticular nucleus (TRN) and participates in nociception. But how the TRN-VB pathway regulates Pain is not fully understood. In the present study, we reported decreased extracellular GABA levels in the VB of rats with CFA-induced Chronic Inflammatory Pain, measured by microdialysis with HPLC analysis. In vitro whole-cell patch-clamp recording showed decreased amplitudes of tonic currents, increased frequencies of mIPSCs, and increased paired-pulse ratios in thalamic slices from Chronic Inflammatory rats (7 days). Microinjection of the GABAAR agonist muscimol and optogenetic activation of the TRN-VB pathway relieved thermal hyperalgesia in Chronic Inflammatory Pain. By contrast, microinjecting the extrasynaptic GABAAR agonist THIP or selective knockout of synaptic GABAAR γ2 subunits aggravated thermal hyperalgesia in the Chronic stage of Inflammatory Pain. Our findings indicate that reduced GABAergic transmission in the VB contributes to thermal hyperalgesia in Chronic Inflammatory Pain, which could be a synaptic target for pharmacotherapy.

Chan Zhang - One of the best experts on this subject based on the ideXlab platform.

  • Erratum: Reduced GABAergic transmission in the ventrobasal thalamus contributes to thermal hyperalgesia in Chronic Inflammatory Pain.
    Scientific Reports, 2017
    Co-Authors: Chan Zhang, Rongxiang Chen, Fei-fei Liao, Fuqiang Xu, Jie Wang, Ming Yi
    Abstract:

    The ventrobasal (VB) thalamus is innervated by GABAergic afferents from the thalamic reticular nucleus (TRN) and participates in nociception. But how the TRN-VB pathway regulates Pain is not fully understood. In the present study, we reported decreased extracellular GABA levels in the VB of rats with CFA-induced Chronic Inflammatory Pain, measured by microdialysis with HPLC analysis. In vitro whole-cell patch-clamp recording showed decreased amplitudes of tonic currents, increased frequencies of mIPSCs, and increased paired-pulse ratios in thalamic slices from Chronic Inflammatory rats (7 days). Microinjection of the GABAAR agonist muscimol and optogenetic activation of the TRN-VB pathway relieved thermal hyperalgesia in Chronic Inflammatory Pain. By contrast, microinjecting the extrasynaptic GABAAR agonist THIP or selective knockout of synaptic GABAAR γ2 subunits aggravated thermal hyperalgesia in the Chronic stage of Inflammatory Pain. Our findings indicate that reduced GABAergic transmission in the VB contributes to thermal hyperalgesia in Chronic Inflammatory Pain, which could be a synaptic target for pharmacotherapy.

  • Reduced GABAergic transmission in the ventrobasal thalamus contributes to thermal hyperalgesia in Chronic Inflammatory Pain.
    Scientific reports, 2017
    Co-Authors: Chan Zhang, Rongxiang Chen, Fei-fei Liao, Jie Wang, Yu Zhang, Feng-yu Liu, Jie Cai, You Wan
    Abstract:

    The ventrobasal (VB) thalamus is innervated by GABAergic afferents from the thalamic reticular nucleus (TRN) and participates in nociception. But how the TRN-VB pathway regulates Pain is not fully understood. In the present study, we reported decreased extracellular GABA levels in the VB of rats with CFA-induced Chronic Inflammatory Pain, measured by microdialysis with HPLC analysis. In vitro whole-cell patch-clamp recording showed decreased amplitudes of tonic currents, increased frequencies of mIPSCs, and increased paired-pulse ratios in thalamic slices from Chronic Inflammatory rats (7 days). Microinjection of the GABAAR agonist muscimol and optogenetic activation of the TRN-VB pathway relieved thermal hyperalgesia in Chronic Inflammatory Pain. By contrast, microinjecting the extrasynaptic GABAAR agonist THIP or selective knockout of synaptic GABAAR γ2 subunits aggravated thermal hyperalgesia in the Chronic stage of Inflammatory Pain. Our findings indicate that reduced GABAergic transmission in the VB contributes to thermal hyperalgesia in Chronic Inflammatory Pain, which could be a synaptic target for pharmacotherapy.

Ming Yi - One of the best experts on this subject based on the ideXlab platform.

  • Erratum: Reduced GABAergic transmission in the ventrobasal thalamus contributes to thermal hyperalgesia in Chronic Inflammatory Pain.
    Scientific Reports, 2017
    Co-Authors: Chan Zhang, Rongxiang Chen, Fei-fei Liao, Fuqiang Xu, Jie Wang, Ming Yi
    Abstract:

    The ventrobasal (VB) thalamus is innervated by GABAergic afferents from the thalamic reticular nucleus (TRN) and participates in nociception. But how the TRN-VB pathway regulates Pain is not fully understood. In the present study, we reported decreased extracellular GABA levels in the VB of rats with CFA-induced Chronic Inflammatory Pain, measured by microdialysis with HPLC analysis. In vitro whole-cell patch-clamp recording showed decreased amplitudes of tonic currents, increased frequencies of mIPSCs, and increased paired-pulse ratios in thalamic slices from Chronic Inflammatory rats (7 days). Microinjection of the GABAAR agonist muscimol and optogenetic activation of the TRN-VB pathway relieved thermal hyperalgesia in Chronic Inflammatory Pain. By contrast, microinjecting the extrasynaptic GABAAR agonist THIP or selective knockout of synaptic GABAAR γ2 subunits aggravated thermal hyperalgesia in the Chronic stage of Inflammatory Pain. Our findings indicate that reduced GABAergic transmission in the VB contributes to thermal hyperalgesia in Chronic Inflammatory Pain, which could be a synaptic target for pharmacotherapy.

Rongxiang Chen - One of the best experts on this subject based on the ideXlab platform.

  • Erratum: Reduced GABAergic transmission in the ventrobasal thalamus contributes to thermal hyperalgesia in Chronic Inflammatory Pain.
    Scientific Reports, 2017
    Co-Authors: Chan Zhang, Rongxiang Chen, Fei-fei Liao, Fuqiang Xu, Jie Wang, Ming Yi
    Abstract:

    The ventrobasal (VB) thalamus is innervated by GABAergic afferents from the thalamic reticular nucleus (TRN) and participates in nociception. But how the TRN-VB pathway regulates Pain is not fully understood. In the present study, we reported decreased extracellular GABA levels in the VB of rats with CFA-induced Chronic Inflammatory Pain, measured by microdialysis with HPLC analysis. In vitro whole-cell patch-clamp recording showed decreased amplitudes of tonic currents, increased frequencies of mIPSCs, and increased paired-pulse ratios in thalamic slices from Chronic Inflammatory rats (7 days). Microinjection of the GABAAR agonist muscimol and optogenetic activation of the TRN-VB pathway relieved thermal hyperalgesia in Chronic Inflammatory Pain. By contrast, microinjecting the extrasynaptic GABAAR agonist THIP or selective knockout of synaptic GABAAR γ2 subunits aggravated thermal hyperalgesia in the Chronic stage of Inflammatory Pain. Our findings indicate that reduced GABAergic transmission in the VB contributes to thermal hyperalgesia in Chronic Inflammatory Pain, which could be a synaptic target for pharmacotherapy.

  • Reduced GABAergic transmission in the ventrobasal thalamus contributes to thermal hyperalgesia in Chronic Inflammatory Pain.
    Scientific reports, 2017
    Co-Authors: Chan Zhang, Rongxiang Chen, Fei-fei Liao, Jie Wang, Yu Zhang, Feng-yu Liu, Jie Cai, You Wan
    Abstract:

    The ventrobasal (VB) thalamus is innervated by GABAergic afferents from the thalamic reticular nucleus (TRN) and participates in nociception. But how the TRN-VB pathway regulates Pain is not fully understood. In the present study, we reported decreased extracellular GABA levels in the VB of rats with CFA-induced Chronic Inflammatory Pain, measured by microdialysis with HPLC analysis. In vitro whole-cell patch-clamp recording showed decreased amplitudes of tonic currents, increased frequencies of mIPSCs, and increased paired-pulse ratios in thalamic slices from Chronic Inflammatory rats (7 days). Microinjection of the GABAAR agonist muscimol and optogenetic activation of the TRN-VB pathway relieved thermal hyperalgesia in Chronic Inflammatory Pain. By contrast, microinjecting the extrasynaptic GABAAR agonist THIP or selective knockout of synaptic GABAAR γ2 subunits aggravated thermal hyperalgesia in the Chronic stage of Inflammatory Pain. Our findings indicate that reduced GABAergic transmission in the VB contributes to thermal hyperalgesia in Chronic Inflammatory Pain, which could be a synaptic target for pharmacotherapy.

Jie Wang - One of the best experts on this subject based on the ideXlab platform.

  • Erratum: Reduced GABAergic transmission in the ventrobasal thalamus contributes to thermal hyperalgesia in Chronic Inflammatory Pain.
    Scientific Reports, 2017
    Co-Authors: Chan Zhang, Rongxiang Chen, Fei-fei Liao, Fuqiang Xu, Jie Wang, Ming Yi
    Abstract:

    The ventrobasal (VB) thalamus is innervated by GABAergic afferents from the thalamic reticular nucleus (TRN) and participates in nociception. But how the TRN-VB pathway regulates Pain is not fully understood. In the present study, we reported decreased extracellular GABA levels in the VB of rats with CFA-induced Chronic Inflammatory Pain, measured by microdialysis with HPLC analysis. In vitro whole-cell patch-clamp recording showed decreased amplitudes of tonic currents, increased frequencies of mIPSCs, and increased paired-pulse ratios in thalamic slices from Chronic Inflammatory rats (7 days). Microinjection of the GABAAR agonist muscimol and optogenetic activation of the TRN-VB pathway relieved thermal hyperalgesia in Chronic Inflammatory Pain. By contrast, microinjecting the extrasynaptic GABAAR agonist THIP or selective knockout of synaptic GABAAR γ2 subunits aggravated thermal hyperalgesia in the Chronic stage of Inflammatory Pain. Our findings indicate that reduced GABAergic transmission in the VB contributes to thermal hyperalgesia in Chronic Inflammatory Pain, which could be a synaptic target for pharmacotherapy.

  • Reduced GABAergic transmission in the ventrobasal thalamus contributes to thermal hyperalgesia in Chronic Inflammatory Pain.
    Scientific reports, 2017
    Co-Authors: Chan Zhang, Rongxiang Chen, Fei-fei Liao, Jie Wang, Yu Zhang, Feng-yu Liu, Jie Cai, You Wan
    Abstract:

    The ventrobasal (VB) thalamus is innervated by GABAergic afferents from the thalamic reticular nucleus (TRN) and participates in nociception. But how the TRN-VB pathway regulates Pain is not fully understood. In the present study, we reported decreased extracellular GABA levels in the VB of rats with CFA-induced Chronic Inflammatory Pain, measured by microdialysis with HPLC analysis. In vitro whole-cell patch-clamp recording showed decreased amplitudes of tonic currents, increased frequencies of mIPSCs, and increased paired-pulse ratios in thalamic slices from Chronic Inflammatory rats (7 days). Microinjection of the GABAAR agonist muscimol and optogenetic activation of the TRN-VB pathway relieved thermal hyperalgesia in Chronic Inflammatory Pain. By contrast, microinjecting the extrasynaptic GABAAR agonist THIP or selective knockout of synaptic GABAAR γ2 subunits aggravated thermal hyperalgesia in the Chronic stage of Inflammatory Pain. Our findings indicate that reduced GABAergic transmission in the VB contributes to thermal hyperalgesia in Chronic Inflammatory Pain, which could be a synaptic target for pharmacotherapy.