scholarly journals A Comparison Study of the Effect on IBS-D Rats among Ginger-Partitioned Moxibustion, Mild Moxibustion, and Laser Moxibustion

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Chao Sun ◽  
Xiaofeng Yang ◽  
Sirui Xie ◽  
Ziqin Zhou ◽  
Guoliang Yu ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Gastrointestinal Disorder ◽  
Transient Receptor Potential Vanilloid ◽  
Therapeutic Effects ◽  
Colon Tissue ◽  
Trpv1 Channels ◽  
Stable Temperature ◽  
Trpv1 Receptors ◽  
Mild Moxibustion

Background. Diarrhea-predominant irritable bowel syndrome (IBS-D) is a functional gastrointestinal disorder that severely affects patients’ life. Moxibustion is believed to be an effective way to treat IBS-D. However, the therapeutic effects and the underlying mechanisms in symptom management of IBS-D by different moxibustion therapies remain unclear. Methods. IBS-D model rats were divided into groups and treated with ginger-partitioned moxibustion (GPM), mild moxibustion (MM), and laser moxibustion (LM) at a temperature of 43°C, respectively. The temperature curves of acupoints were recorded during interventions. The therapeutic effects were evaluated on the basis of general condition, stool, and hematoxylin-eosin staining of the colon tissue. Moreover, the expression of transient receptor potential vanilloid 1 (TRPV1) receptors in both acupoint tissue and colon tissue was analyzed by immunohistochemistry. Results. After moxibustion treatment, the symptoms were improved. The expression of TRPV1 was increased in acupoint tissue and decreased in colon tissue. GPM and MM showed a more significant influence on IBS-D rats compared with LM. The temperature profile of GPM and MM was wave-like, while LM had an almost stable temperature curve. Conclusion. GPM, MM, and LM could improve the symptoms in IBS-D rats. Moxibustion might activate TRPV1 channels in the acupoint tissue and induce acupoint functions, which in turn inhibit the pathological activation state of the colon’s TRPV1, followed by improvements in abdominal pain and diarrheal symptoms. LM with stable temperature might lead to the desensitization of TRPV1 receptors and the tolerance of acupoint. GPM and MM provided dynamic and repetitive thermal stimulations that perhaps induced acupoint sensitization to increase efficacy. Therefore, dynamic and repetitive thermal stimulation is recommended in the application of moxibustion.

Elucidation of the Role of Transient Receptor Potential Vanilloid-1 (TRPV1) Channels in Epileptogenesis

2021 ◽  
Vol 11 ◽  
Author(s):  
Omar M.E. Abdel-Salam
Keyword(s):  
Transient Receptor Potential ◽  
Glutamate Release ◽  
Epileptiform Activity ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Trpv1 Channels ◽  
Trpv1 Receptors ◽  
Transient Receptor

The transient receptor potential vanilloid-1 (TRPV1), previously known as the capsaicin receptor or vanilloid receptor 1 (VR1) is a nonselective cation channel that acts as an integrator of nociceptive information in sensory neurons and their sensory nerve endings with unmyelinated (C) or thin myelinated (Aδ) fibers. It is activated by capsaicin, resiniferatoxin, piperine, noxious heat (> 43ºC), protons, lipoxygenase products, and some endogenous cannabinoids. TRPV1 receptors are also expressed in the brain on neurons, glia cells and pericytes and might be involved in the modulation of epileptogenesis. TRPV1 modulates synaptic plasticity and neurotransmission, mediates long-term depression of glutamate release in the hippocampus and suppress excitatory transmission in dentate gyrus. TRPV1-knockout mice have altered susceptibility to hyperthermic seizures. Studies in vitro showed that capsaicin reduced epileptiform activity but increased neuronal discharge in excitable cells. Capsaicin given via systemic routes at low doses was shown to reduce seizures induced by kainic acid and pentylenetetrazole and to afford neuroprotection of hippocampus in vivo. These effects were associated with reduced oxidative stress and inflammation in brain. In contrast, high doses of capsaicin either elicited or enhanced seizures in animals. In addition, piperine, a TRPV1 agonist, demonstrated anti-epileptic activity in several animal models via a multiplicity of mechanisms. Moreover, non-psychotropic cannabinoids such as cannabidiol and cannabidivarin, the endocannabinoid anandamide, and acetaminophen demonstrated anti-epileptiform activity in vivo and in vitro via mechanisms that might involve TRPV1 receptors. By surveying recent research findings, this review article is intended to present the current research status on the involvement of TRPV1 receptors in epileptogenesis so as to stimulate further investigations into the detailed molecular mechanisms by which capsaicin as well as other chemical modalities impact epileptogenesis via modulating TRPV1 channels. (First online: Apr 12, 2021)

scholarly journals Interactions between Chemesthesis and Taste: Role of TRPA1 and TRPV1

2021 ◽  
Vol 22 (7) ◽  
pp. 3360
Author(s):  
Mee-Ra Rhyu ◽  
Yiseul Kim ◽  
Vijay Lyall
Keyword(s):  
Transient Receptor Potential ◽  
Taste Receptor ◽  
Sensory Nerve ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Trpv1 Channels ◽  
Trigeminal Neurons ◽  
Calcitonin Gene ◽  
Transient Receptor

In addition to the sense of taste and olfaction, chemesthesis, the sensation of irritation, pungency, cooling, warmth, or burning elicited by spices and herbs, plays a central role in food consumption. Many plant-derived molecules demonstrate their chemesthetic properties via the opening of transient receptor potential ankyrin 1 (TRPA1) and transient receptor potential vanilloid 1 (TRPV1) channels. TRPA1 and TRPV1 are structurally related thermosensitive cation channels and are often co-expressed in sensory nerve endings. TRPA1 and TRPV1 can also indirectly influence some, but not all, primary taste qualities via the release of substance P and calcitonin gene-related peptide (CGRP) from trigeminal neurons and their subsequent effects on CGRP receptor expressed in Type III taste receptor cells. Here, we will review the effect of some chemesthetic agonists of TRPA1 and TRPV1 and their influence on bitter, sour, and salt taste qualities.

Intra-arterial instillation of a nociceptive agent modulate cardiorespiratory parameters involving 5-HT3 and TRPV1 receptors in anesthetized rats

2021 ◽  
Vol 21 ◽  
Author(s):  
Sanjeev K. Singh ◽  
M. S. Muthu ◽  
Ravindran Revand ◽  
M. B. Mandal
Keyword(s):  
Transient Receptor Potential ◽  
Sensory Nerve ◽  
Receptor Potential ◽  
Neural Mechanisms ◽  
Transient Receptor Potential Vanilloid ◽  
Anesthetized Rats ◽  
Trpv1 Receptors ◽  
Perivascular Nerves ◽  
Transient Receptor

Background: Since long back, it has been a matter of discussion regarding the role of peripheral blood vessels in regulation of cardiorespiratory (CVR) system. Objective: The role of 5-HT3 and TRPV1 receptors present on perivascular nerves in elicitation of CVR reflexes was examined after intra-arterial instillation of bradykinin in urethane anesthetized rats. Materials and Methods: Femoral artery was cannulated retrogradely and was utilized for the instillation of saline/agonist/antagonist and recording of blood pressure (BP), using a double ported 24G cannula. BP, respiration and ECG were recorded for 30 min after bradykinin (1 µM) in the absence or presence of antagonists. Results: Instillation of bradykinin produced immediate hypotensive (40%), bradycardiac (17%), tachypnoeic (45%) and hyperventilatory (96%) responses of shorter latencies (5-8 s) favoring the neural mechanisms in producing the responses. In lignocaine (2%) pretreated animals, bradykinin-induced hypotensive (10%), bradycardiac (1.7%), tachypnoeic (13%) and hyperventilatory (13%) responses attenuated significantly. Pretreatment with ondansetron (100 µg/kg), 5-HT3-antagonist attenuated the hypotensive (10%), bradycardiac (1.7%), tachypnoeic (11%) and hyperventilatory (11%) responses significantly. Pretreatment with capsazepine (1 mg/kg), transient receptor potential vanilloid 1- antagonist blocked the hypotensive (5%), bradycardiac (1.2%), tachypnoeic (6%) and hyperventilatory (6%) responses significantly. Conclusion: In conclusion, presence of a nociceptive agent in the local segment of an artery evokes vasosensory reflex responses modulating CVR parameters involving TRPV1 and 5-HT3 receptors present on the perivascular sensory nerve terminals in anesthetized rats.

scholarly journals Analgesic Effect of Acetaminophen: A Review of Known and Novel Mechanisms of Action

2020 ◽  
Vol 11 ◽  
Author(s):  
Nobuko Ohashi ◽  
Tatsuro Kohno
Keyword(s):  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Nociceptive Transmission ◽  
Spinal Dorsal ◽  
C Fibers ◽  
Trpv1 Receptors ◽  
The Brain

Acetaminophen is one of the most commonly used analgesic agents for treating acute and chronic pain. However, its metabolism is complex, and its analgesic mechanisms have not been completely understood. Previously, it was believed that acetaminophen induces analgesia by inhibiting cyclooxygenase enzymes; however, it has been considered recently that the main analgesic mechanism of acetaminophen is its metabolization to N-acylphenolamine (AM404), which then acts on the transient receptor potential vanilloid 1 (TRPV1) and cannabinoid 1 receptors in the brain. We also recently revealed that the acetaminophen metabolite AM404 directly induces analgesia via TRPV1 receptors on terminals of C-fibers in the spinal dorsal horn. It is known that, similar to the brain, the spinal dorsal horn is critical to pain pathways and modulates nociceptive transmission. Therefore, acetaminophen induces analgesia by acting not only on the brain but also the spinal cord. In addition, acetaminophen is not considered to possess any anti-inflammatory activity because of its weak inhibition of cyclooxygenase (COX). However, we also revealed that AM404 induces analgesia via TRPV1 receptors on the spinal dorsal horn in an inflammatory pain rat model, and these analgesic effects were stronger in the model than in naïve rats. The purpose of this review was to summarize the previous and new issues related to the analgesic mechanisms of acetaminophen. We believe that it will allow clinicians to consider new pain management techniques involving acetaminophen.

scholarly journals TRPV1 channels and the progesterone receptor Sig-1R interact to regulate pain

2018 ◽  
Vol 115 (7) ◽  
pp. E1657-E1666 ◽  
Author(s):  
Miguel Ortíz-Rentería ◽  
Rebeca Juárez-Contreras ◽  
Ricardo González-Ramírez ◽  
León D. Islas ◽  
Félix Sierra-Ramírez ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Sigma 1 Receptor ◽  
Trpv1 Channels ◽  
Nociceptive Responses ◽  
Sigma 1 ◽  
Transient Receptor ◽  
Thermal Stimuli

The Transient Receptor Potential Vanilloid 1 (TRPV1) ion channel is expressed in nociceptors where, when activated by chemical or thermal stimuli, it functions as an important transducer of painful and itch-related stimuli. Although the interaction of TRPV1 with proteins that regulate its function has been previously explored, their modulation by chaperones has not been elucidated, as is the case for other mammalian TRP channels. Here we show that TRPV1 physically interacts with the Sigma 1 Receptor (Sig-1R), a chaperone that binds progesterone, an antagonist of Sig-1R and an important neurosteroid associated to the modulation of pain. Antagonism of Sig-1R by progesterone results in the down-regulation of TRPV1 expression in the plasma membrane of sensory neurons and, consequently, a decrease in capsaicin-induced nociceptive responses. This is observed both in males treated with a synthetic antagonist of Sig-1R and in pregnant females where progesterone levels are elevated. This constitutes a previously undescribed mechanism by which TRPV1-dependent nociception and pain can be regulated.

scholarly journals Activation of TRPV1 channels leads to stimulation of NKCC1 cotransport in the lens

2018 ◽  
Vol 315 (6) ◽  
pp. C793-C802 ◽  
Author(s):  
Mohammad Shahidullah ◽  
Amritlal Mandal ◽  
Nicholas A. Delamere
Keyword(s):  
Ion Transport ◽  
Transient Receptor Potential ◽  
Ion Homeostasis ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Signaling Mechanism ◽  
Trpv1 Channels ◽  
Trpv1 Antagonist ◽  
Transient Receptor ◽  
Stimulation Of

Lens ion homeostasis is crucial in maintaining water content and, in turn, refractive index and transparency of the multicellular syncytium-like structure. New information is emerging on the regulation of ion transport in the lens by mechanisms that rely on transient receptor potential vanilloid (TRPV) ion channels. We found recently that TRPV1 activation leads to Ca2+/PKC-dependent ERK1/2 signaling. Here, we show that the TRPV1 agonist capsaicin (100 nM) and hyperosmotic solution (350 vs. 300 mosM) each caused an increase of bumetanide-inhibitable Rb uptake by intact porcine lenses and Na-K-2Cl cotransporter 1 (NKCC1) phosphorylation in the lens epithelium. The TRPV1 antagonist A889425 (1 µM) abolished the increases of Rb uptake and NKCC1 phosphorylation in response to hyperosmotic solution. Exposing lenses to hyperosmotic solution in the presence of MEK/ERK inhibitor U0126 (10 µM) or the with-no-lysine kinase (WNK) inhibitor WNK463 (1 µM) also prevented NKCC1 phosphorylation and the Rb uptake responses to hyperosmotic solution. WNK463 did not prevent the increase in ERK1/2 phosphorylation that occurs in response to capsaicin or hyperosmotic solution, suggesting that ERK1/2 activation occurs before WNK activation in the sequence of signaling events. Taken together, the evidence indicates that activation of TRPV1 is a critical early step in a signaling mechanism that responds to a hyperosmotic stimulus, possibly lens shrinkage. By activating ERK1/2 and WNK, TRPV1 activation leads to NKCC1 phosphorylation and stimulation of NKCC1-mediated ion transport.

scholarly journals Pore Helix Domain Is Critical to Camphor Sensitivity of Transient Receptor Potential Vanilloid 1 Channel

2012 ◽  
Vol 116 (4) ◽  
pp. 903-917 ◽  
Author(s):  
Lenka Marsakova ◽  
Filip Touska ◽  
Jan Krusek ◽  
Viktorie Vlachova
Keyword(s):  
Spatial Distribution ◽  
Plasma Membranes ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Structural Basis ◽  
Transient Receptor Potential Vanilloid ◽  
Trpv1 Channel ◽  
Patch Clamp Technique ◽  
Trpv1 Channels ◽  
Transient Receptor

Background The recent discovery that camphor activates and strongly desensitizes the capsaicin-sensitive and noxious heat-sensitive channel transient receptor potential vanilloid subfamily member 1 (TRPV1) has provided new insights and opened up new research paths toward understanding why this naturally occurring monoterpene is widely used in human medicine for its local counter-irritant, antipruritic, and anesthetic properties. However, the molecular basis for camphor sensitivity remains mostly unknown. The authors attempt to explore the nature of the activation pathways evoked by camphor and narrow down a putative interaction site at TRPV1. Methods The authors transiently expressed wild-type or specifically mutated recombinant TRPV1 channels in human embryonic kidney cells HEK293T and recorded cation currents with the whole cell, patch clamp technique. To monitor changes in the spatial distribution of phosphatidylinositol 4,5-bisphosphate, they used fluorescence resonance energy transfer measurements from cells transfected with the fluorescent protein-tagged pleckstrin homology domains of phospholipase C. Results The results revealed that camphor modulates TRPV1 channel through the outer pore helix domain by affecting its overall gating equilibrium. In addition, camphor, which generally is known to decrease the fluidity of cell plasma membranes, may also regulate the activity of TRPV1 by inducing changes in the spatial distribution of phosphatidylinositol-4,5-bisphosphate on the inner leaflet of the plasma membrane. Conclusions The findings of this study provide novel insights into the structural basis for the modulation of TRPV1 channel by camphor and may provide an explanation for the mechanism by which camphor modulates thermal sensation in vivo.

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