The Role of Stress Regulation on Neural Plasticity in Pain Chronification

Li, Xiaoyun; Hu, Li

doi:10.1155/2016/6402942

Cited by 51 publications

(43 citation statements)

References 110 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Functional blockade of glutamatergic neurons in the unilateral LHb was enough to alleviate pT-ION-induced anxiety-like behaviors but not allodynia, as was rescuing the pT-ION-induced downregulation of Tacr3, a gene enriched in the calcium signaling pathway. The anterior cingulate cortex (ACC), prefrontal cortex (PFC), and hippocampus were reported to be related to the induction of negative emotion [25]. Here we found that the downregulation of Tacr3 occurred only in the LHb and not in the ACC, PFC, or hippocampus.…”

Section: Introductionmentioning

confidence: 52%

Tacr3 in the lateral habenula differentially regulates orofacial allodynia and anxiety-like behaviors in a mouse model of trigeminal neuralgia

Cui

Zhang

Chen

et al. 2020

acta neuropathol commun

View full text Add to dashboard Cite

Trigeminal neuralgia (TN) is debilitating and is usually accompanied by mood disorders. The lateral habenula (LHb) is considered to be involved in the modulation of pain and mood disorders, and the present study aimed to determine if and how the LHb participates in the development of pain and anxiety in TN. To address this issue, a mouse model of partial transection of the infraorbital nerve (pT-ION) was established. pT-ION induced stable and long-lasting primary and secondary orofacial allodynia and anxiety-like behaviors that correlated with the increased excitability of LHb neurons. Adeno-associated virus (AAV)-mediated expression of hM4D(Gi) in glutamatergic neurons of the unilateral LHb followed by clozapine-N-oxide application relieved pT-ION-induced anxiety-like behaviors but not allodynia. Immunofluorescence validated the successful infection of AAV in the LHb, and microarray analysis showed changes in gene expression in the LHb of mice showing allodynia and anxiety-like behaviors after pT-ION. Among these differentially expressed genes was Tacr3, the downregulation of which was validated by RT-qPCR. Rescuing the downregulation of Tacr3 by AAV-mediated Tacr3 overexpression in the unilateral LHb significantly reversed pT-ION-induced anxiety-like behaviors but not allodynia. Whole-cell patch clamp recording showed that Tacr3 overexpression suppressed nerve injury-induced hyperexcitation of LHb neurons, and western blotting showed that the pT-ION-induced upregulation of p-CaMKII was reversed by AAVmediated Tacr3 overexpression or chemicogenetic inhibition of glutamatergic neurons in the LHb. Moreover, not only anxiety-like behaviors, but also allodynia after pT-ION were significantly alleviated by chemicogenetic inhibition of bilateral LHb neurons or by bilateral Tacr3 overexpression in the LHb. In conclusion, Tacr3 in the LHb plays a protective role in treating trigeminal nerve injury-induced allodynia and anxiety-like behaviors by suppressing the

show abstract

Section: Introductionmentioning

confidence: 52%

Tacr3 in the lateral habenula differentially regulates orofacial allodynia and anxiety-like behaviors in a mouse model of trigeminal neuralgia

Cui

Zhang

Chen

et al. 2020

acta neuropathol commun

View full text Add to dashboard Cite

show abstract

“…Nociceptive signals are moderated at the level of the spinal cord by descending modulatory neural pathways, which may either facilitate or inhibit their transmission. 21 Chronic stress and chronic pain share neural circuits that operate in the amygdala, the hippocampus and the prefrontal cortex 23 ; and cortisol plays an essential role in the prefrontal cortex-dependent regulation of the hypothalamic-pituitary-adrenal (HPA) axis and in the processing of emotion-related information by the amygdala. 8 It appears that on one hand, long-term exposure to psychosocial stressors brings about an increase in neuronal dendritic arborisation and axonal connections in the amygdala with the upregulation of activity of neuronal pathways for both nociception and stress; and on the other hand, a decrease in dendritic arborisation and axonal connections in the prefrontal cortex and the hippocampus with downregulation of activity of nociceptive and stress inhibitory pathways.…”

Section: Chronic Painmentioning

confidence: 99%

Interrelations between pain, stress and executive functioning

Feller

Ballyram

et al. 2019

British Journal of Pain

View full text Add to dashboard Cite

Aim: The purpose of this narrative review is to discuss the interrelations between pain, stress and executive functions. Implications for practice: Self-regulation, through executive functioning, exerts control over cognition, emotion and behaviour. The reciprocal neural functional connectivity between the prefrontal cortex and the limbic system allows for the integration of cognitive and emotional neural pathways and then for higher-order psychological processes (reasoning, judgement etc.) to generate goal-directed adaptive behaviours and to regulate responses to psychosocial stressors and pain signals. Impairment in cognitive executive functioning may result in poor regulation of stress-, pain- and emotion-related processing of information. Conversely, adverse emotion, pain and stress impair executive functioning. The characteristic of the feedback and feedforward neural connections (quantity and quality) between the prefrontal cortex and the limbic system determine adaptive behaviour, stress response and pain experience.

show abstract

“…While studies constructed a bridge between excessive release of PGs in the menstruation phase and dysmenorrheic pain in PD patients, there is mounting evidence that PD patients are hypersensitive to experimental pain not only when they are experiencing menstrual pain, but also during the pain‐free phase of the menstrual cycle [Iacovides et al, ]. Researchers pointed out that a vicious cycle of painful stimuli caused by uterine cramps may increase nociceptive‐related neuronal input in the brain [Iacovides et al, ; Li and Hu, ], which was associated with structural changes and functional reorganization in pain‐related brain networks [Bajaj et al, ]. This could be a viable explanation for the enhanced pain sensitivity even in the phase when PD patients are not experiencing menstrual pain [Iacovides et al, ; Vincent et al, ].…”

Section: Introductionmentioning

confidence: 99%

Altered white matter microarchitecture in the cingulum bundle in women with primary dysmenorrhea: A tract-based analysis study

Liu

et al. 2017

Hum. Brain Mapp.

Self Cite

View full text Add to dashboard Cite

Primary dysmenorrhea (PD), as characterized by painful menstrual cramps without organic causes, is associated with central sensitization and brain function changes. Previous studies showed the integrated role of the default mode network (DMN) in the pain connectome and its key contribution on how an individual perceives and copes with pain disorders. Here, we aimed to investigate whether the cingulum bundle connecting hub regions of the DMN was disrupted in young women with PD. Diffusion tensor imaging was obtained in 41 PD patients and 41 matched healthy controls (HC) during their periovulatory phase. The production of prostaglandins (PGs) was obtained in PD patients during their pain-free and pain phases. As compared with HC, PD patients had similar scores of pain intensity, anxiety, and depression in their pain-free phase. However, altered white matter properties mainly located in the posterior section of the cingulum bundle were observed in PD. Besides PGs being related to menstrual pain, a close relationship was found between the white matter properties of the cingulum bundle during the pain-free phase and the severity of the menstrual pain in PD patients. Our study suggested that PD had trait changes of white matter integrities in the cingulum bundle that persisted beyond the time of menstruation. We inferred that altered anatomical connections may lead to less-flexible communication within the DMN, and/or between the DMN and other pain-related brain networks, which may result in the central susceptibility to develop chronic pain conditions in PD's later life. Hum Brain Mapp 38:4430-4443, 2017. © 2017 Wiley Periodicals, Inc.

show abstract

The Role of Stress Regulation on Neural Plasticity in Pain Chronification

Cited by 51 publications

References 110 publications

Tacr3 in the lateral habenula differentially regulates orofacial allodynia and anxiety-like behaviors in a mouse model of trigeminal neuralgia

Tacr3 in the lateral habenula differentially regulates orofacial allodynia and anxiety-like behaviors in a mouse model of trigeminal neuralgia

Interrelations between pain, stress and executive functioning

Altered white matter microarchitecture in the cingulum bundle in women with primary dysmenorrhea: A tract-based analysis study

Contact Info

Product

Resources

About