scholarly journals Genetically determined P2X7 receptor pore formation regulates variability in chronic pain sensitivity

2012 ◽  
Vol 18 (4) ◽  
pp. 595-599 ◽  
Author(s):  
Robert E Sorge ◽  
Tuan Trang ◽  
Ruslan Dorfman ◽  
Shad B Smith ◽  
Simon Beggs ◽  
...  
Keyword(s):  
Chronic Pain ◽  
P2x7 Receptor ◽  
Pore Formation ◽  
Pain Sensitivity ◽  
Genetically Determined

scholarly journals CHRONIC PAIN: MEDICO-BIOLOGIC AND SOTSIO-ECONOMIC ASPECTS

2012 ◽  
Vol 67 (9) ◽  
pp. 54-58 ◽  
Author(s):  
N. N. Yakhno ◽  
M. L. Kukushkin
Keyword(s):  
Chronic Pain ◽  
Social Factors ◽  
Pain Sensitivity ◽  
Pain Perception ◽  
Economic Aspects ◽  
Peripheral Neuron ◽  
Genetically Determined

In this article the role of neurobiological, psychological and social factors in pathogenesis of chronic pain is analyzed. The chronic pain is considered not as a symptom of damage of tissue and as independent illness due to non-adequate neuroplasticity of systems involved into regulation of pain sensitivity. The major role in development and maintenance of chronic pain is devoted to the primary genetically determined and/or secondary disturbance of interaction between nociceptive and antinociceptive systems at various levels - from peripheral neuron to central structures – that provides pain perception and painful behaviour development. 

scholarly journals Effect of the duration of chronic low back pain on pain sensitivity of patients undergoing lumbar fusion surgery

Pain medicine ◽  
2021 ◽  
Vol 5 (4) ◽  
pp. 8-15
Author(s):  
Mei-ping Qian ◽  
Mei-rong Dong ◽  
Fang Kang ◽  
Juan Li
Keyword(s):  
Chronic Pain ◽  
Low Back Pain ◽  
Back Pain ◽  
Hospital Stay ◽  
Chronic Low Back Pain ◽  
Pain Sensitivity ◽  
Lumbar Fusion ◽  
Low Back ◽  
Fusion Surgery ◽  
Lumbar Fusion Surgery

Background: chronic low back pain is a serious social problem. In recent years, patients who choose lumbar fusion surgery due to chronic low back pain has been increasing. Pre-existing chronic pain has been associated with severe postoperative pain. In this study, we have sought to prospectively analyze the association between the duration of chronic low back pain and pain sensitivity after lumbar fusion surgery. Methods: 400 patients who underwent lumbar fusion surgery were divided into three groups based on the duration of chronic pain. During the first postoperative day, the maximum pain scores of each patient day and night, the pain scores at the day of discharge, the consumption of postoperative analgesics and the length of hospital stay were recorded. Results: of 400 patients recruited, 369 patients completed the experiment. There was no significant difference in gender, age, height, weight, pre-operative pain at rest, and operation time in the three groups. During the day, the pain sensitivity of the three groups were 1.71 ± 0.66, 2.40 ± 0.74, 2.90 ± 0.80. During the night, the pain sensitivity of the three groups were 3.45 ± 0.81, 4.31 ± 1.06, 4.86 ± 1.05. At the day of discharge, the pain sensitivity of three groups were 1.26 ± 0.46, 1.47 ± 0.58, 1.96 ± 0.64. There were significant differences in pain sensitivity among the three groups during the day and night on the first postoperative day and at the day of discharge (p < 0.05). The length of hospital stay (7.31 ± 1.36 days, 8.82 ± 1.48 days, 9.60 ± 1.61 days) and analgesic consumption (25.04 ± 36.56 mg, 33.52 ± 24.04 mg, 45.15 ± 24.89 mg, morphine equivalent) were also significant differences (p < 0.05). Conclusion: we found the duration of chronic low back pain before lumbar fusion surgery affects patient’ postoperative pain sensitivity, consumption of analgesic drugs and hospital stay. The longer the preoperative chronic pain lasts, the higher the postoperative VAS score is, the more analgesic drugs were consumed, and the longer hospital stay is.

scholarly journals The effects of propranolol on heart rate variability and quantitative, mechanistic, pain profiling: a randomized placebo-controlled crossover study

2018 ◽  
Vol 18 (3) ◽  
pp. 479-489 ◽  
Author(s):  
Kristian Kjær Petersen ◽  
Hjalte Holm Andersen ◽  
Masato Tsukamoto ◽  
Lincoln Tracy ◽  
Julian Koenig ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Chronic Pain ◽  
Pain Sensitivity ◽  
Experimental Pain ◽  
Central Pain ◽  
Healthy Male ◽  
Pain Pathways ◽  
Β Blocker ◽  
Chronic Pain Conditions

AbstractBackground and aimsThe autonomic nervous system (ANS) is capable of modulating pain. Aberrations in heart rate variability (HRV), reflective of ANS activity, are associated with experimental pain sensitivity, chronic pain, and more recently, pain modulatory mechanisms but the underlying mechanisms are still unclear. HRV is lowered during experimental pain as well as in chronic pain conditions and HRV can be increased by propranolol, which is a non-selective β-blocker. Sensitization of central pain pathways have been observed in several chronic pain conditions and human mechanistic pain biomarkers for these central pain pathways include temporal summation of pain (TSP) and conditioned pain modulation (CPM). The current study aimed to investigate the effect of the β-blocker propranolol, and subsequently assessing the response to standardized, quantitative, mechanistic pain biomarkers.MethodsIn this placebo-controlled, double-blinded, randomized crossover study, 25 healthy male volunteers (mean age 25.6 years) were randomized to receive 40 mg propranolol and 40 mg placebo. Heart rate, blood pressure, and HRV were assessed before and during experimental pain tests. Cuff pressure pain stimulation was used for assessment of pain detection (cPDTs) and pain tolerance (cPTTs) thresholds, TSP, and CPM. Offset analgesia (OA) was assessed using heat stimulation.ResultsPropranolol significantly reduced heart rate (p<0.001), blood pressure (p<0.02) and increased HRV (p<0.01) compared with placebo. No significant differences were found comparing cPDT (p>0.70), cPTT (p>0.93), TSP (p>0.70), OA-effect (p>0.87) or CPM (p>0.65) between propranolol and placebo.ConclusionsThe current study demonstrated that propranolol increased HRV, but did not affect pressure pain sensitivity or any pain facilitatory or modulatory outcomes.ImplicationsAnalgesic effects of propranolol have been reported in clinical pain populations and the results from the current study could indicate that increased HRV from propranolol is not associated with peripheral and central pain pathways in healthy male subjects.

Distinct changes in chronic pain sensitivity and oxytocin receptor expression in a new rat model (Wisket) of schizophrenia

2020 ◽  
Vol 714 ◽  
pp. 134561 ◽  
Author(s):  
László Banki ◽  
Alexandra Büki ◽  
Gyongyi Horvath ◽  
Gabriella Kekesi ◽  
Gyongyi Kis ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Rat Model ◽  
Pain Sensitivity ◽  
Oxytocin Receptor ◽  
Receptor Expression

scholarly journals Basal Pain Sensitivity does not Predict the Outcome of Multidisciplinary Chronic Pain Treatment

Pain Medicine ◽  
2015 ◽  
Vol 16 (8) ◽  
pp. 1635-1642 ◽  
Author(s):  
Ruth Ruscheweyh ◽  
Katharina Dany ◽  
Martin Marziniak ◽  
Ingrid Gralow
Keyword(s):  
Chronic Pain ◽  
Pain Sensitivity ◽  
Pain Treatment ◽  
Chronic Pain Treatment

scholarly journals Epidermal Growth Factor Facilitates Epinephrine Inhibition of P2X7-Receptor-Mediated Pore Formation and Apoptosis: A Novel Signaling Network

Endocrinology ◽  
2005 ◽  
Vol 146 (1) ◽  
pp. 164-174 ◽  
Author(s):  
Liqin Wang ◽  
Ying-Hong Feng ◽  
George I. Gorodeski
Keyword(s):  
Plasma Membrane ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
P2x7 Receptor ◽  
Pore Formation ◽  
Cell Number ◽  
Epidermal Growth ◽  
Phosphoinositide 3 Kinase ◽  
Dependent Mechanism

Epidermal growth factor (EGF), epinephrine, and the P2X7 receptor system regulate growth of human uterine cervical epithelial cells, but little is known about how these systems intercommunicate in exerting their actions. The objective of this study was to understand the mechanisms of EGF and epinephrine regulation of growth of cervical cells. Treatment of cultured CaSki cells with 0.2 nm EGF increased cell number via a PD98059-sensitive pathway. Treatment with 2 nm epinephrine increased cell number, and the effect was facilitated by cotreatment with EGF. Whereas the effect of EGF alone involved up-regulation of [3H]-thymidine incorporation and an increase in cell proliferation, the effect of epinephrine was mediated by inhibition of apoptosis. Epinephrine inhibited apoptosis induced by the P2X7 receptor ligand 2′,3′-0-(4-benzoylbenzoyl)-ATP, by attenuation of P2X7 receptor plasma membrane pore formation. Cotreatment with EGF facilitated epinephrine effect via a phosphoinositide 3-kinase-dependent mechanism. CaSki cells express the β2-adrenoceptor, and the epinephrine antiapoptotic effect could be mimicked by β2-adrenoceptor agonists and by activators of adenylyl cyclase. Likewise, the effect could be blocked by β2-adrenoceptor blockers and by the inhibitor of protein kinase-A H-89. Western immunoblot analysis revealed that epinephrine decreased the levels of the glycosylated 85-kDa form of the P2X7 receptor and increased receptor degradation, and that EGF potentiated these effects of epinephrine. EGF did not affect cellular levels of the β2-adrenoceptor. In contrast, EGF, acting via the EGF receptor, augmented β2-adrenoceptor recycling, and it inhibited β2-adrenoceptor internalization via a phosphoinositide 3-kinase-dependent mechanism. We conclude that, in cervical epithelial cells, EGF has a dual role: as mitogen, acting via the MAPK/MAPK kinase pathway, and as an antiapoptotic factor by facilitating epinephrine effect and resulting in greater expression of β2-adrenoceptors in the plasma membrane. These findings underscore a novel signaling network of communication between the receptor tyrosine kinases, the G protein-coupled receptors, and the purinergic P2X7 receptor.

Validation of the Pain Sensitivity Questionnaire in chronic pain patients

Pain ◽  
2012 ◽  
Vol 153 (6) ◽  
pp. 1210-1218 ◽  
Author(s):  
Ruth Ruscheweyh ◽  
Benedikt Verneuer ◽  
Katharina Dany ◽  
Martin Marziniak ◽  
Anne Wolowski ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Pain Sensitivity ◽  
Chronic Pain Patients ◽  
Pain Patients
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