Neurotransmitter alterations in the anterior cingulate cortex in Crohn's disease patients with abdominal pain: A preliminary MR spectroscopy study

Lv, Kun; Song, Wenwen; Tang, Rui; Pan, Zhi-Yong; Zhang, Yong; Xu, Yi; Lv, Bin; Fan, Yi‐Ming; Xu, Maosheng

doi:10.1016/j.nicl.2018.09.008

Cited by 28 publications

(29 citation statements)

References 58 publications

(62 reference statements)

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“…Glutamate levels were significantly increased in the thalamic ventral posterolateral nucleus and ACC in neuropathic pain rats [23,24]. Clinical research using MRS also showed a significant absolute glutamate increase in the insular cortex, cingulate cortex and thalamus during several pain conditions [25][26][27][28]. In our MRS results, increased glutamate releasing in the thalamus during the CCI-induced neuropathic pain, which was caused by excitatory neurons.…”

Section: Discussionsupporting

confidence: 61%

Altered thalamic neurotransmitters metabolism and functional connectivity during the development of chronic constriction injury induced neuropathic pain

Wang

Huang

et al. 2020

Biol Res

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Background: To investigate the thalamic neurotransmitters and functional connections in the development of chronic constriction injury (CCI)-induced neuropathic pain. Methods: The paw withdrawal threshold was measured by mechanical stimulation the right hind paw with the von frey hair in the rats of CCI-induced neuropathic pain. The N-acetylaspartate (NAA) and Glutamate (Glu) in thalamus were detected by magnetic resonance spectrum (MRS) process. The thalamic functional connectivity with other brain regions was scanned by functional magnetic resonance image (fMRI). Results: The paw withdrawal threshold of the ipsilateral side showed a noticeable decline during the pathological process. Increased concentrations of Glu and decreased levels of NAA in the thalamus were significantly correlated with mechanical allodynia in the neuropathic pain states. The thalamic regional homogeneity (ReHo) decreased during the process of neuropathic pain. The functional connectivity among the thalamus with the insula and somatosensory cortex were significantly increased at different time points (7, 14, 21 days) after CCI surgery. Conclusion: Our study suggests that dynamic changes in thalamic NAA and Glu levels contribute to the thalamic functional connection hyper-excitation during CCI-induced neuropathic pain. Enhanced thalamus-insula functional connection might have a significant effect on the occurrence of neuropathic pain.

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Section: Discussionsupporting

confidence: 61%

Altered thalamic neurotransmitters metabolism and functional connectivity during the development of chronic constriction injury induced neuropathic pain

Wang

Huang

et al. 2020

Biol Res

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“…Except for intestinal mucosa injury, the commensal microbiotagut-brain axis has been found to be both ecologically and functionally perturbed in colitis and related pain [52]. The pain processing of colitis patients with abdominal pain is tightly associated with gut-derived neurochemical metabolites [53]. A further study on the specific mechanism of brain-gut-network in colitis-associated pain has been conducted in our laboratory.…”

Section: Limitationsmentioning

confidence: 94%

Pioglitazone Attenuates Experimental Colitis-Associated Hyperalgesia through Improving the Intestinal Barrier Dysfunction

et al. 2020

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Impaired intestinal mucosal integrity during colitis involves the peroxisome proliferator-activated receptor-γ (PPARγ), an important anti-inflammatory factor in intestinal mucosa homoeostasis, which is a potential target in colitis. Recurrent chronic pain is a vital pathogenetic feature of colitis. Nevertheless, potential functions of PPARγ in the colitis-associated hyperalgesia remain unclear. This study aimed to investigate biological roles of pioglitazone in relieving colitis-associated pain hypersensitivity by a PPARγ tight junction protein-dependent mechanism during the course of dextran sodium sulfate (DSS)-induced intestinal inflammation. The DSS-induced colitis model was generated in C57BL/6 mice. Changes in colitis induced the injury of intestinal mucosal barrier and hyperalgesia after a 6-day treatment of pioglitazone (25 mg/kg, IP injection) were assessed through immunofluorescent, hematoxylin and eosin (H&E) staining, western blot analysis, and determination of paw withdrawal mechanical threshold. A significant reduction of paw withdrawal mechanical threshold occurred after DSS treatment. Follow-up data showed that systematic administration of PPARγ agonist pioglitazone ameliorated the DSS-induced colitis and the development of colitis-associated hyperalgesia by repairing the intestinal mucosal barrier. The tight junction proteins ZO-1 and Claudin-5 were upregulated by PPARγ signaling, which in turn promoted the improvement of intestinal barrier function. Moreover, pioglitazone inhibited phosphorylation of ERK and NF-κB in the colon and decreased the levels of inflammatory cytokines in both colon spine tissues. Furthermore, systemically pioglitazone treatment inhibited the activation of microglia and astrocytes, as well as DSSinduced phosphorylation of NR2B subunit in spinal cord, which was correspondingly consistent with the pain behavior. Pioglitazone ameliorates DSS-induced colitis and attenuates colitis-associated mechanical hyperalgesia, with improving integrity of the Yulin Huang and Chenchen Wang contributed equally to this work.

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“…Especially, higher levels of glu/cre and glx/cre (glx: glutamate and glutamine) in the anterior cingulate cortex (ACC) were demonstrated in chronic pain patients (Kameda et al, 2018; Ito et al, 2017). A study with Crohn's disease patients with abdominal pain also revealed higher levels of ACC glu/cre, than patients without abdominal pain and healthy controls (Lv et al, 2018). This indicates that magnetic resonance spectroscopy is a valid method to obtain information of pain related metabolic changes in the brain.…”

Section: Introductionmentioning

confidence: 99%

“…Magnetic resonance spectroscopy has previously been used to show that patients with chronic pain have a different neurometabolic status compared to healthy controls (Kameda et al, 2018; Ito et al, 2017; Feraco et al, 2011; Lv et al, 2018). Especially, higher levels of glu/cre and glx/cre (glx: glutamate and glutamine) in the anterior cingulate cortex (ACC) were demonstrated in chronic pain patients (Kameda et al, 2018; Ito et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Cingulate glutamate levels associate with pain in chronic pancreatitis patients

Hansen

Muthulingam

Drewes

et al. 2019

NeuroImage: Clinical

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Aims Emerging evidence show that patients with chronic pancreatitis (CP) and abdominal pain have structural and functional alterations in the central nervous system. The aim was to investigate cerebral metabolic signatures in CP and the associations to various risk factors/clinical characteristics and patient outcomes. Methods Magnetic resonance spectroscopy was used to measure brain metabolites in the anterior cingulate cortex (ACC), insula, prefrontal cortex and the parietal region in patients with CP and healthy controls. Subgroup analyses based on disease characteristics (alcoholic etiology of CP, diabetes and opioid treatment) were performed. Finally, relations to abdominal pain symptoms and quality of life scores were explored. Results Thirty-one patients with CP (mean age 58.5 ± 9.2 years) and 23 healthy controls (54.6 ± 7.8 years) were included. Compared to healthy controls, patients had increased glutamate/creatine (glu/cre) levels in the ACC (1.24 ± 0.17 vs. 1.13 ± 0.21, p = .045) and reduced parietal N -acetylaspartate/creatine (NAA/cre) levels (1.44 ± 0.18 vs. 1.54 ± 0.12, p = .027). Patients with alcoholic etiology of CP had significant lower levels of parietal NAA/cre as compared to patients without alcoholic etiology and healthy controls ( p < .006). Patients with a high level of ACC glu/cre reported more severe abdominal pain than their counterparts with a low level of ACC glu/cre (pain score 4.1 ± 2.7 vs.1.9 ± 2.3, p = .039). Conclusions Cerebral spectroscopy revealed novel and complementary information on central pain mechanisms and alcohol mediated toxic effects in patients with CP. Our data suggest that cingulate glutamate levels associate with the patients clinical pain symptoms, while parietal NAA levels more likely associate with an alcoholic etiology of CP.

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Neurotransmitter alterations in the anterior cingulate cortex in Crohn's disease patients with abdominal pain: A preliminary MR spectroscopy study

Cited by 28 publications

References 58 publications

Altered thalamic neurotransmitters metabolism and functional connectivity during the development of chronic constriction injury induced neuropathic pain

Altered thalamic neurotransmitters metabolism and functional connectivity during the development of chronic constriction injury induced neuropathic pain

Pioglitazone Attenuates Experimental Colitis-Associated Hyperalgesia through Improving the Intestinal Barrier Dysfunction

Cingulate glutamate levels associate with pain in chronic pancreatitis patients

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