Role of Epigenetic Mechanisms in Chronic Pain

Mauceri, Daniela

doi:10.3390/cells11162613

Cited by 15 publications

(12 citation statements)

References 134 publications

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“…Therefore, EE might restore cellular changes that control excitability, so that the neuronal network function is improved, protecting the brain against deleterious effects of insults, including chronic pain. Indeed, chronic pain leads to changes in transcriptional patterns ( Su et al, 2021 ; Wang et al, 2021 ; Dai et al, 2022 ), together with epigenetic changes ( Mauceri, 2022 ), along the pain neuraxis that could contribute to alterations in excitability and network activity, all of which could be potentially reversed by EE. Overall, EE is a promising approach for restoring neuronal excitability in rodents and may have potential applications for the treatment of neurological disorders in humans ( Kimura et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Environmental enrichment promotes resilience to neuropathic pain-induced depression and correlates with decreased excitability of the anterior cingulate cortex

Falkowska

Ntamati

Nevian

et al. 2023

Front. Behav. Neurosci.

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Depression is a common comorbidity of chronic pain with many patients being affected. However, efficient pharmacological treatment strategies are still lacking. Therefore, it is desirable to find additional alternative approaches. Environmental enrichment has been suggested as a method to alleviate pain-induced depression. However, the neuronal mechanisms of its beneficial effects are still elusive. The anterior cingulate cortex (ACC) plays a central role in processing pain-related negative affect and chronic pain-induced plasticity in this region correlates with depressive symptoms. We studied the consequences of different durations of environmental enrichment on pain sensitivity and chronic pain-induced depression-like behaviors in a mouse model of neuropathic pain. Furthermore, we correlated the behavioral outcomes to the activity levels of pyramidal neurons in the ACC by analyzing their electrophysiological properties ex vivo. We found that early exposure to an enriched environment alone was not sufficient to cause resilience against pain-induced depression-like symptoms. However, extending the enrichment after the injury prevented the development of depression and reduced mechanical hypersensitivity. On the cellular level, increased neuronal excitability was associated with the depressive phenotype that was reversed by the enrichment. Therefore, neuronal excitability in the ACC was inversely correlated to the extended enrichment-induced resilience to depression. These results suggest that the improvement of environmental factors enhanced the resilience to developing chronic pain-related depression. Additionally, we confirmed the association between increased neuronal excitability in the ACC and depression-like states. Therefore, this non-pharmacological intervention could serve as a potential treatment strategy for comorbid symptoms of chronic pain.

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Section: Discussionmentioning

confidence: 99%

Environmental enrichment promotes resilience to neuropathic pain-induced depression and correlates with decreased excitability of the anterior cingulate cortex

Falkowska

Ntamati

Nevian

et al. 2023

Front. Behav. Neurosci.

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“…Genetic and epigenetic biomarkers that modulate neuroinflammation and are involved in peripheral and central sensitization appear to play an important role in the transition from acute to CPSP [3,121]. However, so far only a few specific causal mechanisms have been identified and implications, such as biomarkers for stratification of patients at risk, are still lacking [122,123]. Many studies on genetics argue against the association of single key genes with CPSP and, therefore, an important role as biomarkers is not defined yet [8,124].…”

Section: Key Pointsmentioning

confidence: 99%

Mechanisms inherent in acute-to-chronic pain after surgery – risk, diagnostic, predictive, and prognostic factors

Rosenberger,

Segelcke,

Pogatzki-Zahn

2023

Current Opinion in Supportive &Amp; Palliative Care

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Purpose of review Acute pain is an expected consequence of a surgery, but it is far from being well controlled, due to its complex bio-psycho-social nature. One major complication of acute pain is its risk of persistency beyond healing. This so-called chronic post-surgical pain (CPSP) is defined as new or increased pain due to surgery that lasts for at least 3 months after surgery. CPSP is frequent and constitutes an important socioeconomic challenge with significant impact on patients’ quality of life. Its importance has been recognized by its inclusion in the eleventh version of the ICD (International Classification of Diseases). Recent findings Evidence for most pharmacological and non-pharmacological interventions preventing CPSP is inconsistent. Identification of associated patient-related factors, such as psychosocial aspects, comorbidities, surgical factors, pain trajectories, or biomarkers may allow stratification and selection of treatment options based on underlying individual mechanisms. Consequently, the identification of patients at risk and implementation of individually tailored, preventive, multimodal treatment to reduce the risk of transition from acute to chronic pain is facilitated. Summary This review will give an update on current knowledge on mechanism-based risk, prognostic and predictive factors for CPSP in adults, and preventive and therapeutic approaches, and how to use them for patient stratification in the future.

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“…Hasmi [35] Shift of pain processing from nociceptive to emotional circuits with chronification of pain Consider and discuss emotional components during the patient's education and care, especially as pain persists.…”

Section: Neuralmentioning

confidence: 99%

The Biology of Chronic Pain and Its Implications for Pain Neuroscience Education: State of the Art

Zimney

Bogaert

Louw

2023

JCM

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Pain is an individualized experience for the person suffering from chronic pain. Significant strides have been made in the last few decades in understanding various biological changes that coincide with chronic pain. This state-of-the-art overview looks at the current evidence related to the biology of chronic pain and the implications these findings have on the delivery of pain neuroscience education (PNE). The paper summarizes the various (epi)genetic, neural, endocrine, and immune factors discovered and explored in the scientific literature concerning chronic pain. Each of these biological factors has various implications for the content and delivery of PNE. We discuss the future directions these biological factors have for the clinical implementation of PNE by linking the importance of behavior change, optimizing the learning environment, and using an individualized multimodal treatment approach with PNE. In addition, future directions for research of PNE based on these biological factors are provided with importance placed on individualized patient-centered care and how PNE can be used with traditional modes of care and growing trends with other care methods. PNE was originally and continues to be rooted in understanding chronic pain biology and how that understanding can improve patient care and outcomes.

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Role of Epigenetic Mechanisms in Chronic Pain

Cited by 15 publications

References 134 publications

Environmental enrichment promotes resilience to neuropathic pain-induced depression and correlates with decreased excitability of the anterior cingulate cortex

Environmental enrichment promotes resilience to neuropathic pain-induced depression and correlates with decreased excitability of the anterior cingulate cortex

Mechanisms inherent in acute-to-chronic pain after surgery – risk, diagnostic, predictive, and prognostic factors

The Biology of Chronic Pain and Its Implications for Pain Neuroscience Education: State of the Art

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