Activation of Parvalbumin Neurons in the Rostro-Dorsal Sector of the Thalamic Reticular Nucleus Promotes Sensitivity to Pain in Mice

Liu, Jing; Zhang, Mengqi; Wu, Xu; Lazarus, Michael; Chérasse, Yoan; Yuan, Mao-Yun; Huang, Zhi‐Li; Li, Ruixi

doi:10.1016/j.neuroscience.2017.10.013

Cited by 23 publications

(17 citation statements)

References 43 publications

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“…Chemogenetic and optogenetic activation of parvalbumin positive neurons in the rostro-dorsal TRN increased pain sensitivity by inhibiting neurons in the anterior dorsal nucleus and in the paratenial thalamic nucleus (176). These findings suggest an interaction of TRN and the limbic system, which in turn affects pain sensation.…”

Section: Intrathalamic Interactionsmentioning

confidence: 75%

“…There is a remarkably high density of GABAergic neurons in the adjoining TRN, which receives input from the cerebral cortex and thalamus and sends inhibitory GABAergic projections back to the thalamus. Spe-cific chemogenetic activation of GABAergic neurons in the TRN has recently been reported to facilitate nociception, suggesting that the TRN participates in a pro-nociceptive loop instead of inhibiting pain (176). In contrast, in another study, optogenetic activation of afferents from the TRN to one of its target zones, the ventrobasal thalamus, inhibited inflammatory hypersensitivity, putatively via restoration of thalamic GABA levels that are depleted in inflammatory pain (321).…”

Section: Gabaergic Control Of Brain Circuits In Painmentioning

confidence: 90%

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Cellular Circuits in the Brain and Their Modulation in Acute and Chronic Pain

Kuner

2021

Physiological Reviews

213

162

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Chronic, pathological pain remains a global health problem and a challenge to basic and clinical sciences. A major obstacle to preventing, treating or reverting chronic pain has been that the nature of neural circuits underlying the diverse components of the complex, multidimensional experience of pain is not well understood. Moreover, chronic pain involves diverse maladaptive plasticity processes, which have not been decoded mechanistically in terms of involvement of specific circuits and cause-effect relationships. This review aims to discuss recent advances in our understanding of circuit connectivity in the mammalian brain at the level of regional contributions and specific cell types in acute and chronic pain. A major focus is placed on functional dissection of sub-neocortical brain circuits using optogenetics, chemogenetics and imaging technological tools in rodent models with a view towards decoding sensory, affective and motivational-cognitive dimensions of pain. The review summarizes recent breakthroughs and insights on structure-function properties in nociceptive circuits and higher order sub-neocortical modulatory circuits involved in aversion, learning, reward and mood and their modulation by endogenous GABAergic inhibition, noradrenergic, cholinergic, dopaminergic, serotonergic and peptidergic pathways. The knowledge of neural circuits and their dynamic regulation via functional and structural plasticity will be beneficial towards designing and improving targeted therapies.

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Section: Intrathalamic Interactionsmentioning

confidence: 75%

Section: Gabaergic Control Of Brain Circuits In Painmentioning

confidence: 90%

Cellular Circuits in the Brain and Their Modulation in Acute and Chronic Pain

Kuner

2021

Physiological Reviews

213

162

View full text Add to dashboard Cite

show abstract

“…The calcium-binding protein, parvalbumin alpha, maintains the exchange of intracellular Ca 2+ . Activation of parvalbumin neurons in the cerebral cortex has been shown to increase pain sensitivity [37], and dorsal horn parvalbumin neurons are considered gate-keepers of touch-evoked pain that alleviate mechanical allodynia in neuropathic pain [38]. However, the role of parvalbumin alpha in muscle tissue function related to musculoskeletal pain or MTrP-related pain is not clear.…”

Section: Discussionmentioning

confidence: 99%

Proteins and Signaling Pathways Response to Dry Needling Combined with Static Stretching Treatment for Chronic Myofascial Pain in a RAT Model: An Explorative Proteomic Study

Huang

Barbero

et al. 2019

IJMS

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A quantitative proteomic analysis of the response to dry needling combined with static stretching treatment was performed in a rat model of active myofascial trigger points (MTrPs). 36 rats were divided into a model group (MG), a stretching group (SG) and a dry needling combined with stretching group (SDG). We performed three biological replicates to compare large-scale differential protein expression between groups by tandem mass tag (TMT) labeling technology based on nanoscale liquid chromatography mass spectrometry analysis (LC–MS/MS). Hierarchical clustering, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment and protein-protein interaction network analyses were performed for the general characterization of overall enriched proteins. For validation of the results of TMT, the candidate proteins were verified by parallel reaction monitoring (PRM) analysis. 285 differentially expressed proteins between groups were identified and quantified. Tight junction pathway played a dominant role in dry needling combined with static stretching treatment for the rat model of active MTrPs. Three candidate proteins, namely actinin alpha 3, calsequestrin-1 and parvalbumin alpha, were further validated, consistent with the results of LC–MS/MS. This is the first proteomics-based study to report the therapeutic mechanism underlying dry needling and static stretching treatment for MTrPs. Further functional verification of the potential signaling pathways and the enriched proteins is warranted.

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“…Mice were of a mixed CD1/B6 genetic background. All mice have been previously described as having loxP-flanked alleles in Efnb2 [ 30 ], which were combined with the parvalbumin (PV)-Cre mice [ 31 ].…”

Section: Methodsmentioning

confidence: 99%

RNA-seq co-expression network analysis reveals anxiolytic behavior of mice with Efnb2 knockout in parvalbumin+ neurons

Sun

Chen

et al. 2021

Mol Brain

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Anxiety disorders are the most common psychiatric disorders, and the change in the activity of the prefrontal cortex (PFC) is considered as the underlying pathological mechanism. Parvalbumin-expressing (PV+) inhibition contributes to the overall activity of the PFC. However, the molecular mechanism underlying the excitation-inhibition imbalance of PV+ neurons in the PFC is unknown. Efnb2 is a membrane-bound molecule that plays an important role in the nervous system through binding the Eph receptor. To investigate whether the loss of Efnb2 in PV+ affects anxiety, we examined the behavior of wild type and Efnb2 in PV+ neurons knockout (KO) mice. We monitored the defensive responses to aversive stimuli of elevated plus maze (EPM) and found that KO mice exhibited obvious fearless and anxiolytic behaviors. To further investigate the underlying regulatory mechanism, we performed RNA sequencing, analyzed the differentially expressed genes (DEGs), and constructed the weighted gene co-expression network analysis (WGCNA). The WGCNA identified 12 characteristic modules. Among them, the MEgreen module showed the most significant correlation with KO mice of EPM stimuli. The Gene Ontology enrichment and the Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that this was related to the distal axon, Ras signaling pathway and insulin signaling pathway. Furthermore, the whole-cell voltage clamp recordings also proved that Efnb2 gene knock-out could affect synaptic function. Together with the transcriptomic analysis of mice with Efnb2 knockout on PV+ neurons, our findings suggest that Efnb2 gene in the PV+ neuron of PFC may be a crucial factor for fear and anxiety, which provide an insight into anxiety pathophysiology.

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Activation of Parvalbumin Neurons in the Rostro-Dorsal Sector of the Thalamic Reticular Nucleus Promotes Sensitivity to Pain in Mice

Cited by 23 publications

References 43 publications

Cellular Circuits in the Brain and Their Modulation in Acute and Chronic Pain

Cellular Circuits in the Brain and Their Modulation in Acute and Chronic Pain

Proteins and Signaling Pathways Response to Dry Needling Combined with Static Stretching Treatment for Chronic Myofascial Pain in a RAT Model: An Explorative Proteomic Study

RNA-seq co-expression network analysis reveals anxiolytic behavior of mice with Efnb2 knockout in parvalbumin+ neurons

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