Altered synaptic connections and inhibitory network of the primary somatosensory cortex in chronic pain

Kim, Yoo Rim; Kim, Sang Jeong

doi:10.4196/kjpp.2022.26.2.69

Cited by 10 publications

(7 citation statements)

References 56 publications

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“…The posterior central gyrus is also known as the primary sensory cortex (S1). Both human and animal experiments have shown that maladaptive changes in S1 are a characteristic feature of neuropathic pain [32,33] . Studies have demonstrated that changes occur in the structure and function of S1 in patients with phantom limb pain (PLP) [34] Complex regional pain syndrome (CRPS) [35] and spinal cord injury (SCI) [36] .…”

Section: Discussionmentioning

confidence: 99%

Abnormal sensorimotor network in brain functional connectivity in herpes zoster and postherpetic neuralgia patients

Jiang,

Yan,

Xie

et al. 2024

Preprint

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OBJECTIVE: This study aimed to investigate the changes in resting-state functional connectivity (rsFC) of the sensorimotor network(SMN) in patients with herpes zoster(HZ) and postherpetic neuralgia patients(PHN). Then, We applied machine learning to distinguish PHN/HZ patients from healthy controls(HC). METHODS: HZ (n=53), PHN (n=57), and HC (n=50) were included, and resting-state functional magnetic resonance imaging (rs-fMRI) was performed on them. Seed-based and ROI-to-ROI analyses were applied to evaluate connectivity inside and between the SMN and other voxels throughout the brain. After that, we used machine learning to separate patients with PHN/HZ from those with HC. RESULTS: Compared to HC, there was a substantial reduction in functional connectivity between the lateral SMN (R), lateral SMN (L), and superior SMN in PHN patients. There was a disruption of rsFC between SMN subregions and several brain regions (insula, parietal, occipital, and superior frontal gyrus) in PHN. These damaged FCs were linked positively with clinical data (such as mood scores, disease duration, and VAS scores). Furthermore, We discovered that the rsFC value of SMN could successfully classify PHN patients from other types of pain with an accuracy of 85.7% when applied to a machine-learning approach. CONCLUSION: Significant changes occurred in the rsFC of SMN in HZ and PHN. Suggesting that the role of SMN in HZ/PHN may help understand the pathophysiology and development of these diseases.

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Section: Discussionmentioning

confidence: 99%

Abnormal sensorimotor network in brain functional connectivity in herpes zoster and postherpetic neuralgia patients

Jiang,

Yan,

Xie

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…The S1 is a brain region critical in the processing of pain signaling that has been reported to show functional or structural changes in chronic pain conditions [ 43 ]. The S1 of chronic pain patients was actively displayed by fMRI [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Induces Bilateral S1 and ACC Epigenetic Regulation of Genes in a Mouse Model of Neuropathic Pain

et al. 2023

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Clinical and animal studies have shown that acupuncture may benefit controlling neuropathic pain. However, the underlying molecular mechanisms are poorly understood. In a well-established mouse unilateral tibial nerve injury (TNI) model, we confirmed the efficacy of electroacupuncture (EA) in reducing mechanical allodynia and measured methylation and hydroxy-methylation levels in the primary somatosensory cortex (S1) and anterior cingulate cortex (ACC), two cortical regions critically involved in pain processing. TNI resulted in increased DNA methylation of both the contra- and ipsilateral S1, while EA only reduced contralateral S1 methylation. RNA sequencing of the S1 and ACC identified differentially expressed genes related to energy metabolism, inflammation, synapse function, and neural plasticity and repair. One week of daily EA decreased or increased the majority of up- or downregulated genes, respectively, in both cortical regions. Validations of two greatly regulated genes with immunofluorescent staining revealed an increased expression of gephyrin in the ipsilateral S1 after TNI was decreased by EA; while TNI-induced increases in Tomm20, a biomarker of mitochondria, in the contralateral ACC were further enhanced after EA. We concluded that neuropathic pain is associated with differential epigenetic regulations of gene expression in the ACC and S1 and that the analgesic effect of EA may involve regulating cortical gene expression.

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“…Therefore, the predominant somatosensory cortex projections to the Gr originate from S1-HL, aligning anatomically with somatotopically organized ascending input. Projections from the primary somatosensory cortex, which exhibits hyperexcitability and neuroplasticity during chronic pain [71][72][73] , may represent a relevant source for descending modulation of Gr activity during neuropathic pain.…”

Section: Gr Vpl-pns and Inhibitory Neurons Are Differentially Innerva...mentioning

confidence: 99%

The Dorsal Column Nuclei Scale Mechanical Sensitivity in Naive and Neuropathic Pain States

Upadhyay,

Gradwell,

Vajtay

et al. 2024

Preprint

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SUMMARYTactile perception relies on reliable transmission and modulation of low-threshold information as it travels from the periphery to the brain. During pathological conditions, tactile stimuli can aberrantly engage nociceptive pathways leading to the perception of touch as pain, known as mechanical allodynia. Two main drivers of peripheral tactile information, low-threshold mechanoreceptors (LTMRs) and postsynaptic dorsal column neurons (PSDCs), terminate in the brainstem dorsal column nuclei (DCN). Activity within the DRG, spinal cord, and DCN have all been implicated in mediating allodynia, yet the DCN remains understudied at the cellular, circuit, and functional levels compared to the other two. Here, we show that the gracile nucleus (Gr) of the DCN mediates tactile sensitivity for low-threshold stimuli and contributes to mechanical allodynia during neuropathic pain. We found that the Gr contains local inhibitory interneurons in addition to VPL-projecting neurons, which are differentially innervated by primary afferents and spinal inputs. Functional manipulations of these distinct Gr neuronal populations resulted in bidirectional changes to tactile sensitivity, but did not affect noxious mechanical or thermal sensitivity. During neuropathic pain, silencing Gr projection neurons or activating Gr inhibitory neurons was able to reduce tactile hypersensitivity, and enhancing inhibition was able to ameliorate paw withdrawal signatures of neuropathic pain, like shaking. Collectively, these results suggest that the Gr plays a specific role in mediating hypersensitivity to low-threshold, innocuous mechanical stimuli during neuropathic pain, and that Gr activity contributes to affective, pain-associated phenotypes of mechanical allodynia. Therefore, these brainstem circuits work in tandem with traditional spinal circuits underlying allodynia, resulting in enhanced signaling of tactile stimuli in the brain during neuropathic pain.

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Altered synaptic connections and inhibitory network of the primary somatosensory cortex in chronic pain

Cited by 10 publications

References 56 publications

Abnormal sensorimotor network in brain functional connectivity in herpes zoster and postherpetic neuralgia patients

Abnormal sensorimotor network in brain functional connectivity in herpes zoster and postherpetic neuralgia patients

Electroacupuncture Induces Bilateral S1 and ACC Epigenetic Regulation of Genes in a Mouse Model of Neuropathic Pain

The Dorsal Column Nuclei Scale Mechanical Sensitivity in Naive and Neuropathic Pain States

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