Possible involvement of TRPV1 and TRPV4 in nociceptive stimulation- induced nocifensive behavior and neuroendocrine response in mice

Ishikura, Toru; Suzuki, Hitoshi; Shoguchi, K; Koreeda, Yuki; Aritomi, Takafumi; Matsuura, Takanori; Yoshimura, Mitsuhiro; Ohkubo, Jun‐ichi; Maruyama, Takashi; Kawasaki, Makoto; Ohnishi, Hideo; Sakai, Akinori; Mizuno, Atsuko; Ueta, Yoichi

doi:10.1016/j.brainresbull.2015.08.004

Cited by 9 publications

(6 citation statements)

References 60 publications

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“…The latter exhibit hearing impairment [86]; altered heat and pain sensation [2,41] impaired pressure sensation [55,85]; altered thirst responses [38]; and increased susceptibility to obesity [60]. Furthermore, these channels are exquisitely present on the skin keratinocytes; therefore, they possess the ability to sense noxious heat and pain stimuli [34,77]. In the rat dorsal root ganglia, TRPV4 channel is co-expressed with substance P and calcitonin gene-related peptide [26], and activation of these channels results in the release of nociceptive peptides (CGRP and substance P) and contributes to the transduction of mechanical stimuli to induce mechanical hyperalgesia [26,56].…”

Section: Introductionmentioning

confidence: 98%

TRPV4 channels: physiological and pathological role in cardiovascular system

Randhawa

Jaggi

2015

Basic Res Cardiol

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TRPV4 channels are non-selective cation channels permeable to Ca(2+), Na(+), and Mg(2+) ions. Recently, TRPV4 channels have received considerable attention as these channels are widely expressed in the cardiovascular system including endothelial cells, cardiac fibroblasts, vascular smooth muscles, and peri-vascular nerves. Therefore, these channels possibly play a pivotal role in the maintenance of cardiovascular homeostasis. TRPV4 channels critically regulate flow-induced arteriogenesis, TGF-β1-induced differentiation of cardiac fibroblasts into myofibroblasts, and heart failure-induced pulmonary edema. These channels also mediate hypoxia-induced increase in proliferation and migration of pulmonary artery smooth muscle cells and progression of pulmonary hypertension. These channels also maintain flow-induced vasodilation and preserve vascular function by directly activating Ca(2+)-dependent KCa channels. Furthermore, these may also induce vasodilation and maintain blood pressure indirectly by evoking the release of NO, CGRP, and substance P. The present review discusses the evidences and the potential mechanisms implicated in diverse responses including arteriogenesis, cardiac remodeling, congestive heart failure-induced pulmonary edema, pulmonary hypertension, flow-induced dilation, regulation of blood pressure, and hypoxic preconditioning.

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Section: Introductionmentioning

confidence: 98%

TRPV4 channels: physiological and pathological role in cardiovascular system

Randhawa

Jaggi

2015

Basic Res Cardiol

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“…Recently, it was found that TRPV4 is also expressed in oligodendrocyte precursor cells (OPCs) and promotes OPC proliferation (Ohashi et al, 2018 ). TRPV4 is activated by a broad range of stimuli, such as physical factors, endogenous and exogenous chemical factors and low pH, and affects a variety of physiological processes, including inflammation (Garcia-Elias et al, 2014 ; Ishikura et al, 2015 ). Significant infrasound-induced astrocytic and microglial activation promotes an increase inTRPV4 expression and the release of the proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor α (TNF-α), which are responsible for infrasound-induced neuronal apoptosis (Shi et al, 2013 ).…”

Section: Introductionmentioning

confidence: 99%

TRPV4 Inhibition Improved Myelination and Reduced Glia Reactivity and Inflammation in a Cuprizone-Induced Mouse Model of Demyelination

Wang

et al. 2018

Front. Cell. Neurosci.

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The inhibition of demyelination and the promotion of remyelination are both considerable challenges in the therapeutic process for many central nervous system (CNS) diseases. Increasing evidence has demonstrated that neuroglial activation and neuroinflammation are responsible for myelin sheath damage during demyelinating disorders. It has been revealed that the nonselective cation channel transient receptor potential vanilloid 4 (TRPV4) profoundly affects a variety of physiological processes, including inflammation. However, its roles and mechanisms in demyelination have remained unclear. Here, for the first time, we found that there was a significant increase in TRPV4 in the corpus callosum in a demyelinated mouse model induced by cuprizone (CPZ). RN-1734, a TRPV4-antagonist, clearly alleviated demyelination and inhibited glial activation and the production of tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) without altering the number of olig2-positive cells. In vitro, RN-1734 treatment clearly inhibited the influx of calcium and decreased the levels of IL-1β and TNF-α in lipopolysaccharide (LPS)-activated microglial cells by suppressing NF-κB P65 phosphorylation. Apoptosis of oligodendrocyte induced by LPS-activated microglia was also alleviated by RN-1734. The results suggest that activation of TRPV4 in microglia is involved in oligodendrocyte apoptosis through the activation of the NF-κB signaling pathway, thus revealing a new mechanism of CNS demyelination.

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“…The sections for L4 were determined based on Figure 116 of the Rat Brain in Stereotaxic Coordinates atlas by Paxinos and Watson (32), and the images were obtained using a digital camera (DS-L2, DS-Fi1; Nikon Corp.). Fos-immunoreactive (ir) cells in lamina I and II of both ipsilateral and contralateral L4 spinal dorsal horns were counted manually with each captured image, as described previously (31,(33)(34)(35)(36). Three sections of L4 were counted for each animal, and the results were averaged for each group at each evaluation time (n = 5-6 per group and evaluation time).…”

Section: Fos Labeling On Spinal Cord Sectionsmentioning

confidence: 99%

“…Two, two, and six sections containing the SON, PVN, and anterior pituitary, respectively, were used from each rat to determine the autoradiography density. 35 S 3 ′ -endlabeled deoxyoligonucleotides that were complementary to the transcripts encoding OXT, AVP, CRH, and POMC were used (OXT probe sequence, 5 ′ -CTC GGA GAA GGC AGA CTC AGG GTC GCA GGC-3 ′ ; AVP probe sequence, 5 ′ -GCA CTG TCA GCA GCC CTG AAC GGA CCA CAG TGG TAC-3 ′ ; CRH probe sequence, 5 ′ -CAG TTT CCT GTT GCT GTG AGC TTG CTG AGC TAA CTG CTC TGC CCT GGC-3 ′ ; and POMC probe sequence, 5 ′ -TGG CTG CTC TCC AGG CAC CAGCTC CAC ACA TCT ATG GAG G-3 ′ ). The probe was 3 ′ -end labeled with terminal deoxynucleotidyl transferase and [ 35 S] deoxy-ATP.…”

Section: Fos Colocalization With Oxt/avpmentioning

confidence: 99%

Acute Mono-Arthritis Activates the Neurohypophysial System and Hypothalamo-Pituitary Adrenal Axis in Rats

et al. 2020

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Various types of acute/chronic nociceptive stimuli cause neuroendocrine responses such as activation of the hypothalamo-neurohypophysial [oxytocin (OXT) and arginine vasopressin (AVP)] system and hypothalamo-pituitary adrenal (HPA) axis. Chronic multiple-arthritis activates the OXT/AVP system, but the effects of acute mono-arthritis on the OXT/AVP system in the same animals has not been simultaneously evaluated. Further, AVP, not corticotropin-releasing hormone (CRH), predominantly activates the HPA axis in chronic multiple-arthritis, but the participation of AVP in HPA axis activation in acute mono-arthritis remains unknown. Therefore, we aimed to simultaneously evaluate the effects of acute mono-arthritis on the activity of the OXT/AVP system and the HPA axis. In the present study, we used an acute mono-arthritic model induced by intra-articular injection of carrageenan in a single knee joint of adult male Wistar rats. Acute mono-arthritis was confirmed by a significant increase in knee diameter in the carrageenan-injected knee and a significant decrease in the mechanical nociceptive threshold in the ipsilateral hind paw. Immunohistochemical analysis revealed that the number of Fos-immunoreactive (ir) cells in the ipsilateral lamina I-II of the dorsal horn was significantly increased, and the percentage of OXT-ir and AVP-ir neurons expressing Fos-ir in both sides of the supraoptic (SON) and paraventricular nuclei (PVN) was increased in acute mono-arthritic rats. in situ hybridization histochemistry revealed that levels of OXT mRNA and AVP hnRNA in the SON and PVN, CRH mRNA in the PVN, and proopiomelanocortin mRNA in the anterior pituitary were also significantly increased in acute mono-arthritic rats. Further, plasma OXT, AVP, and corticosterone levels were significantly increased in acute mono-arthritic rats. These results suggest that acute mono-arthritis activates ipsilateral nociceptive afferent pathways at the spinal level and causes simultaneous and integrative activation of the OXT/AVP system. In addition, the HPA axis is activated by both AVP and CRH in acute mono-arthritis with a distinct pattern compared to that in chronic multiple-arthritis.

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Possible involvement of TRPV1 and TRPV4 in nociceptive stimulation- induced nocifensive behavior and neuroendocrine response in mice

Cited by 9 publications

References 60 publications

TRPV4 channels: physiological and pathological role in cardiovascular system

TRPV4 channels: physiological and pathological role in cardiovascular system

TRPV4 Inhibition Improved Myelination and Reduced Glia Reactivity and Inflammation in a Cuprizone-Induced Mouse Model of Demyelination

Acute Mono-Arthritis Activates the Neurohypophysial System and Hypothalamo-Pituitary Adrenal Axis in Rats

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