Spontaneous Pain Disrupts Ventral Hippocampal CA1-Infralimbic Cortex Connectivity and Modulates Pain Progression in Rats with Peripheral Inflammation

Ma, Longyu; Yue, Lupeng; Zhang, Yuqi; Wang, Yue; Han, Bingxuan; Cui, Shuang; Liu, Fengyu; Wan, You; Yi, Ming

doi:10.1016/j.celrep.2019.10.002

Cited by 49 publications

(39 citation statements)

References 76 publications

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“…Future exploration of other cortical regions that respond to transient nociceptive stimulation will allow testing the contribution of structures other than primary sensorimotor cortices to GBOs measured at both epidural and scalp levels. The last caveat is particularly relevant when considering that GBOs whose magnitude tracks the time-varying fluctuations of the intensity of tonic pain in healthy subjects (Schulz et al, 2015) and in patients with chronic pain (Zhou et al, 2018;May et al, 2019) have been described to originate from the prefrontal cortex and cerebellum, and not from the primary sensorimotor cortices (Schulz et al, 2015;Zhou et al, 2018;Ma et al, 2019;May et al, 2019). This discrepancy might dovetail with the difference of pain types between the above-mentioned studies and the current study, which is also reflected in the different patterns of brain activation observed during chronic pain vs. transient cutaneous pain (Mouraux and Iannetti, 2018, their Fig.…”

Section: Nociceptive-induced Gbos Reflect Spiking Of S1 Interneuronsmentioning

confidence: 99%

The Neural Origin of Nociceptive-Induced Gamma-Band Oscillations

Yue

Iannetti

2020

J. Neurosci.

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Gamma-band oscillations (GBOs) elicited by transient nociceptive stimuli are one of the most promising biomarkers of pain across species. Still, whether these GBOs reflect stimulus encoding in the primary somatosensory cortex (S1) or nocifensive behavior in the primary motor cortex (M1) is debated. Here we recorded neural activity simultaneously from the brain surface as well as at different depths of the bilateral S1/M1 in freely-moving male rats receiving nociceptive stimulation. GBOs measured from superficial layers of S1 contralateral to the stimulated paw not only had the largest magnitude, but also showed the strongest temporal and phase coupling with epidural GBOs. Also, spiking of superficial S1 interneurons had the strongest phase coherence with epidural GBOs. These results provide the first direct demonstration that scalp GBOs, one of the most promising pain biomarkers, reflect neural activity strongly coupled with the fast spiking of interneurons in the superficial layers of the S1 contralateral to the stimulated side.

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Section: Nociceptive-induced Gbos Reflect Spiking Of S1 Interneuronsmentioning

confidence: 99%

The Neural Origin of Nociceptive-Induced Gamma-Band Oscillations

Yue

Iannetti

2020

J. Neurosci.

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“…Depression is associated with smaller hippocampal volumes and changes in either the activation or connectivity of neural networks (Etkin et al, 2015;Ma et al, 2019). Depression also increases the level of inflammatory factors in the hippocampus (Fasick et al, 2015), downregulates BDNF (Krishnan and Nestler, 2008), and impairs synaptic plasticity (Otte et al, 2016), all of which contribute to the development and long-term pathophysiology of depression.…”

Section: Introductionmentioning

confidence: 99%

Wfs1 and Related Molecules as Key Candidate Genes in the Hippocampus of Depression

et al. 2021

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BackgroundDepression is a prevalent mental disorder, which is difficult to diagnose and treat due to its unclear pathogenic mechanisms. The discovery of novel and effective therapeutic targets for depression is urgently needed. The hippocampus is a crucial region involved in depression and has been a therapeutic target for many antidepressants. Thus, it is beneficial for comprehensive research to be carried out on the molecular mechanisms of the hippocampus involved in the pathogenesis of depression. This study aims to investigate the differentially expressed genes (DEG) in the hippocampus in a chronic unpredictable mild stress (CUMS) mouse model.MethodThe study obtained GSE84183 from the GEO database. The R language screened the differential expression genes (DEG) in the hippocampus tissue of depressed mice, and the enrichment pathways of DEGs were analyzed. A protein-protein interaction (PPI) network was constructed in the STRING database and visualized in Cytoscape software. MicroRNAs for these DEGs were obtained from TarBase and mortar base databases, and transcription factors (TF) related to DEG were predicted from the ENCODE database. Both networks used the visual analysis platform NetworkAnalyst. Finally, the microRNA-TF network was integrated based on the above two networks and imported into Cytoscape for further analysis.ResultsThis study screened 325 differentially expressed genes, containing 42 downregulated genes and 283 upregulated genes. Most of these genes are enriched in the cell cycle and the chemokine signaling pathway. Meanwhile, Wfs1, one of the top ten DEGs, was identified as the key regulator of the cell cycle and the participator in the highest number of modules screened out in PPI networks. Wfs1-related molecules, including UBTF, mmu-mir-17-5p, and mmu-mir-7b-5p, were therefore screened out. Furthermore, we confirmed the downregulation of Wfs1 and upregulation of UBTF/mmu-mir-17-5p/mmu-mir-7b-5p in the hippocampus of the CUMS mouse model. Our data indicate that Wfs1 and related molecules were predicted to be associated with the pathological process of depression. This research provided potential new molecular targets of stress-induced depression.

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“…It was shown that excitability of infralimbic neurons is significantly suppressed in chronic pain [Chung et al, 2017]. Hippocampal BDNF overexpression accelerates recovery from inflammatory pain and reduces spontaneous pain following the recovery of electrophysiological parame- ters in ventral hippocampal CA1-infralimbic cortex connectivity [Ma et al, 2019]. Along with a decrease in BDNF, we observed an increase in the neurotrophic factor NT-3.…”

Section: Discussionmentioning

confidence: 61%

Neuropathic Pain Causes a Decrease in the Dendritic Tree Complexity of Hippocampal CA3 Pyramidal Neurons

Tyrtyshnaia

Manzhulo

Konovalova

et al. 2019

Cells Tissues Organs

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The International Pain Association defines neuropathic pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage." Recent studies show that chronic neuropathic pain causes both morphological and functional changes within brain structures. Due to the impact of supraspinal centers on pain signal processing, patients with chronic pain often suffer from depression, anxiety, memory impairment, and learning disabilities. Changes in hippocampal neuronal and glial plasticity can play a substantial role in the development of these symptoms. Given the special role of the CA3 hippocampal area in chronic stress reactions, we suggested that this region may undergo significant morphological changes as a result of persistent pain. Since the CA3 area is involved in the implementation of hippocampus-dependent memory, changes in the neuronal morphology can cause cognitive impairment observed in chronic neuropathic pain. This study aimed to elucidate the structural and plastic changes within the hippocampus associated with dendritic tree atrophy of CA3 pyramidal neurons in mice with chronic sciatic nerve constric-tion. Behavioral testing revealed impaired working and long-term memory in mice with a chronic constriction injury. Using the Golgi-Cox method, we revealed a decrease in the number of branches and dendritic length of CA3 pyramidal neurons. The dendritic spine number was decreased, predominantly due to a reduction in mushroom spines. An immunohistochemical study showed changes in astro-and microglial activity, which could affect the morphology of neurons both directly and indirectly via the regulation of neurotrophic factor synthesis. Using ELISA, we found a decrease in brain-derived neurotrophic factor production and an increase in neurotrophin-3 production. Morphological and biochemical changes in the CA3 area are accompanied by impaired working and long-term memory of animals. Thus, we can conclude that morphological and biochemical changes within the CA3 hippocampal area may underlie the cognitive impairment in neuropathic pain.

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Spontaneous Pain Disrupts Ventral Hippocampal CA1-Infralimbic Cortex Connectivity and Modulates Pain Progression in Rats with Peripheral Inflammation

Cited by 49 publications

References 76 publications

The Neural Origin of Nociceptive-Induced Gamma-Band Oscillations

The Neural Origin of Nociceptive-Induced Gamma-Band Oscillations

Wfs1 and Related Molecules as Key Candidate Genes in the Hippocampus of Depression

Neuropathic Pain Causes a Decrease in the Dendritic Tree Complexity of Hippocampal CA3 Pyramidal Neurons

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