scholarly journals Impaired Nociception and Inflammatory Pain Sensation in Mice Lacking the Prokineticin Receptor PKR1: Focus on Interaction between PKR1 and the Capsaicin Receptor TRPV1 in Pain Behavior

2006 ◽  
Vol 26 (25) ◽  
pp. 6716-6727 ◽  
Author(s):  
L. Negri ◽  
R. Lattanzi ◽  
E. Giannini ◽  
M. Colucci ◽  
F. Margheriti ◽  
...  
Keyword(s):  
Inflammatory Pain ◽  
Pain Behavior ◽  
Pain Sensation ◽  
Capsaicin Receptor

scholarly journals Dermal macrophages set pain sensitivity by modulating tissue NGF levels through SNX25–Nrf2 signaling

2021 ◽  
Author(s):  
Tatsuhide Tanaka ◽  
Hiroaki Okuda ◽  
Yuki Terada ◽  
Ayami Isonishi ◽  
Masahiro Kitabatake ◽  
...  
Keyword(s):  
Pain Sensitivity ◽  
Pain Behavior ◽  
Mrna Synthesis ◽  
Pain Sensation ◽  
Key Factors ◽  
Transgenic Mouse Line ◽  
Sorting Nexin ◽  
Peripheral Neurons ◽  
Peripheral Sensory ◽  
Transplantation Experiments

Abstract Crosstalk between peripheral neurons and immune cells plays important roles in pain sensation. We identified sorting nexin 25 (Snx25) as a pain-modulating gene in a transgenic mouse line with reduced pain behavior. Snx25 conditional-KO (cKO) in monocyte/macrophage-lineage cells but not in the peripheral sensory neurons reduced pain responses in both normal and neuropathic conditions. Cross transplantation experiments of bone marrows between cKO and wild type (WT) mice revealed that cKO macrophages caused dull phenotype in WT mice and WT macrophages in turn increased pain behavior in cKO mice. SNX25 in dermal macrophages enhances NGF (one of the key factors in pain sensation) production by inhibiting ubiquitin-mediated degradation of Nrf2, a transcription factor that activates Ngf mRNA synthesis. We conclude that dermal macrophages set pain sensitivity by producing and secreting NGF into the dermis in addition to their host defense functions.

scholarly journals TRPV1 Responses in the Cerebellum Lobules V, VIa and VII Using Electroacupuncture Treatment for Inflammatory Hyperalgesia in Murine Model

2020 ◽  
Vol 21 (9) ◽  
pp. 3312 ◽  
Author(s):  
Chanya Inprasit ◽  
Yi-Wen Lin
Keyword(s):  
Inflammatory Pain ◽  
The Body ◽  
Pain Sensation ◽  
Inflammatory Hyperalgesia ◽  
Protein Levels ◽  
Important Symptom ◽  
Zusanli Acupoint ◽  
Transient Receptor ◽  
Electroacupuncture Treatment

Inflammatory pain sensation is an important symptom which protects the body against additional tissue damage and promotes healing. Discovering long-term and effective treatments for pain remains crucial in providing efficient healthcare. Electroacupuncture (EA) is a successful therapy used for pain relief. We aimed to investigate effects and mechanisms of Complete Freund’s Adjuvant (CFA)-inducing inflammatory pain in the cerebellum, and the inhibition of this inflammatory hyperalgesia using EA at Zusanli acupoint (ST36). The results display a significant increase in mechanical and thermal sensitivities in the CFA and CFA + SHAM groups, which was significantly reduced in the CFA+EA and CFA + KO groups. This evidence was substantiated in the protein levels observed using immunoblotting, and presented with significant escalations after CFA inducing inflammatory hyperalgesia in CFA and CFA + SHAM groups. Then, they were significantly attenuated by EA in the CFA + EA group. Furthermore, the CFA + transient receptor vanilloid member 1 (TRPV1)−/− group indicated similar significant decreases of protein expression. Additionally, a concomitant overexpression in lobule VIa was also observed in immunofluorescence. These consequences suggest that CFA-induced inflammatory pain provokes modifications in cerebellum lobules V, VIa and VII, which can subsequently be regulated by EA treatment at the ST36 through its action on TRPV1 and related molecular pathways.

Spider toxins activate the capsaicin receptor to produce inflammatory pain

Nature ◽  
2006 ◽  
Vol 444 (7116) ◽  
pp. 208-212 ◽  
Author(s):  
Jan Siemens ◽  
Sharleen Zhou ◽  
Rebecca Piskorowski ◽  
Tetsuro Nikai ◽  
Ellen A. Lumpkin ◽  
...  
Keyword(s):  
Inflammatory Pain ◽  
Capsaicin Receptor ◽  
Spider Toxins

Pain behavior without pain sensation

Pain ◽  
2020 ◽  
Vol 161 (3) ◽  
pp. 502-508
Author(s):  
Koichi Hagiwara ◽  
Luis Garcia-Larrea ◽  
Léon Tremblay ◽  
Alexandra Montavont ◽  
Hélène Catenoix ◽  
...  
Keyword(s):  
Pain Behavior ◽  
Pain Sensation

scholarly journals The analgesic effect of refeeding on acute and chronic inflammatory pain

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jeong-Yun Lee ◽  
Grace J. Lee ◽  
Pa Reum Lee ◽  
Chan Hee Won ◽  
Doyun Kim ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Inflammatory Pain ◽  
Analgesic Effect ◽  
Cannabinoid Receptor ◽  
Pain Behavior ◽  
Spontaneous Pain ◽  
Second Phase ◽  
Pain Model ◽  
Chronic Inflammatory Pain ◽  
Effect Of Food

AbstractPain is susceptible to various cognitive factors. Suppression of pain by hunger is well known, but the effect of food intake after fasting (i.e. refeeding) on pain remains unknown. In the present study, we examined whether inflammatory pain behavior is affected by 24 h fasting and 2 h refeeding. In formalin-induced acute inflammatory pain model, fasting suppressed pain behavior only in the second phase and the analgesic effect was also observed after refeeding. Furthermore, in Complete Freund’s adjuvant-induced chronic inflammatory pain model, both fasting and refeeding reduced spontaneous pain response. Refeeding with non-calorie agar produced an analgesic effect. Besides, intraperitoneal (i.p.) administration of glucose after fasting, which mimics calorie recovery following refeeding, induced analgesic effect. Administration of opioid receptor antagonist (naloxone, i.p.) and cannabinoid receptor antagonist (SR 141716, i.p.) reversed fasting-induced analgesia, but did not affect refeeding-induced analgesia in acute inflammatory pain model. Taken together, our results show that refeeding produce analgesia in inflammatory pain condition, which is associated with eating behavior and calorie recovery effect.

scholarly journals Overview of Neurological Mechanism of Pain Profile Used for Animal “Pain-Like” Behavioral Study with Proposed Analgesic Pathways

2020 ◽  
Vol 21 (12) ◽  
pp. 4355 ◽  
Author(s):  
Mun Fei Yam ◽  
Yean Chun Loh ◽  
Chuan Wei Oo ◽  
Rusliza Basir
Keyword(s):  
Pain Management ◽  
Inflammatory Pain ◽  
Vital Role ◽  
Future Research ◽  
Tail Flick ◽  
Behavioral Study ◽  
Pain Sensation ◽  
Analgesic Drug ◽  
Animal Pain ◽  
Study Methodology

Pain is the most common sensation installed in us naturally which plays a vital role in defending us against severe harm. This neurological mechanism pathway has been one of the most complex and comprehensive topics but there has never been an elaborate justification of the types of analgesics that used to reduce the pain sensation through which specific pathways. Of course, there have been some answers to curbing of pain which is a lifesaver in numerous situations—chronic and acute pain conditions alike. This has been explored by scientists using pain-like behavioral study methodologies in non-anesthetized animals since decades ago to characterize the analgesic profile such as centrally or peripherally acting drugs and allowing for the development of analgesics. However, widely the methodology is being practiced such as the tail flick/Hargreaves test and Von Frey/Randall–Selitto tests which are stimulus-evoked nociception studies, and there has rarely been a complete review of all these methodologies, their benefits and its downside coupled with the mechanism of the action that is involved. Thus, this review solely focused on the complete protocol that is being adapted in each behavioral study methods induced by different phlogogenic agents, the different assessment methods used for phasic, tonic and inflammatory pain studies and the proposed mechanism of action underlying each behavioral study methodology for analgesic drug profiling. It is our belief that this review could significantly provide a concise idea and improve our scientists’ understanding towards pain management in future research.

scholarly journals Electroacupuncture Ameliorates Chronic Inflammatory Pain-Related Anxiety by Activating PV Interneurons in the Anterior Cingulate Cortex

2021 ◽  
Vol 15 ◽  
Author(s):  
Fangbing Shao ◽  
Junfan Fang ◽  
Mengting Qiu ◽  
Sisi Wang ◽  
Danning Xi ◽  
...  
Keyword(s):  
Anterior Cingulate Cortex ◽  
Inflammatory Pain ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Aminobutyric Acid ◽  
Anxiety And Depression ◽  
Pain Sensation ◽  
Pain Model ◽  
Chronic Inflammatory Pain ◽  
Underlying Mechanisms

Chronic inflammatory pain is a common clinical disease that tends to be associated with negative emotions such as anxiety and depression. The anterior cingulate cortex (ACC) is involved in pain and pain-related anxiety, and γ-aminobutyric acid (GABA)-ergic interneurons play an important role in chronic pain and anxiety. Electroacupuncture (EA) has good analgesic and antianxiety effect, but the underlying mechanisms have not yet been fully elucidated. In this study, we established a chronic inflammatory pain model and observed that this model induced anxiety-like behaviors and decreased the numbers of parvalbumin (PV) and somatostatin (SOM) positive cells. Activation of PV but not SOM interneurons by chemogenetic techniques alleviated anxiety-like behaviors and pain sensation. EA treatment improved pain sensation, anxiety-like behaviors and increased the number of PV- positive cells in the ACC, but did not affect on the number of SOM-positive cells in the ACC. Moreover, specific inhibition of PV interneurons by chemogenetic methods reversed the analgesic and antianxiety effects of EA. These results suggest that EA ameliorates chronic inflammatory pain and pain-related anxiety by upregulating PV but not SOM interneurons in the ACC.

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