Deficits in visceral pain and hyperalgesia of mice with a disruption of the tachykinin NK1 receptor gene

Laird, Jennifer M.A.; Olivar, Teresa; Roza, Carolina; Felipe, Carmen De; Hunt, Stephen P.; Cerveró, Fernando

doi:10.1016/s0306-4522(00)00148-2

Cited by 183 publications

(110 citation statements)

References 42 publications

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“…The peripheral terminals of TRPV1-expressing nociceptors innervate most organs and tissues. TRPV1 expressed in the peripheral nervous system functions to integrate multiple noxious stimuli, ultimately leading to the release of neuropeptides, such as calcitonin gene-related peptide (CGRP) and substance P. These neuropeptides elicit pain and neurogenic inflammatory responses (14)(15)(16)(17)(18). TRPV1 is also expressed in the CNS, including the spinal cord, striatum, hippocampus, cerebellum, and amygdala (19)(20)(21)(22)(23).…”

Section: T He Endogenous Lipid N-arachidonoyl Dopamine (Nada)mentioning

confidence: 99%

N-Arachidonoyl Dopamine Modulates Acute Systemic Inflammation via Nonhematopoietic TRPV1

Lawton

Tran

et al. 2017

The Journal of Immunology

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N-Arachidonoyl dopamine (NADA) is an endogenous lipid that potently activates the transient receptor potential vanilloid 1 (TRPV1), which mediates pain and thermosensation. NADA is also an agonist of cannabinoid receptors 1 and 2. We have reported that NADA reduces the activation of cultured human endothelial cells by LPS and TNF-α. Thus far, in vivo studies using NADA have focused on its neurologic and behavioral roles. In this article, we show that NADA potently decreases in vivo systemic inflammatory responses and levels of the coagulation intermediary plasminogen activator inhibitor 1 in three mouse models of inflammation: LPS, bacterial lipopeptide, and polymicrobial intra-abdominal sepsis. We also found that the administration of NADA increases survival in endotoxemic mice. Additionally, NADA reduces blood levels of the neuropeptide calcitonin gene-related peptide but increases the neuropeptide substance P in LPS-treated mice. We demonstrate that the anti-inflammatory effects of NADA are mediated by TRPV1 expressed by nonhematopoietic cells and provide data suggesting that neuronal TRPV1 may mediate NADA’s anti-inflammatory effects. These results indicate that NADA has novel TRPV1-dependent anti-inflammatory properties and suggest that the endovanilloid system might be targeted therapeutically in acute inflammation.

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Section: T He Endogenous Lipid N-arachidonoyl Dopamine (Nada)mentioning

confidence: 99%

N-Arachidonoyl Dopamine Modulates Acute Systemic Inflammation via Nonhematopoietic TRPV1

Lawton

Tran

et al. 2017

The Journal of Immunology

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“…Moreover, Ca 2ϩ influx into capsaicin-sensitive primary sensory neurons, which occurs in inflammation (Linhart et al, 2003), results in the production of anandamide, the amount of which is comparable with that evoking TRPV1-mediated excitation of primary sensory neurons after PKA, PKC, and PLC activation in the cells (Premkumar and Ahern, 2000;Chuang et al, 2001;De Petrocellis et al, 2001;Ahluwalia et al, 2003a,b). Anandamide, through TRPV1, evokes action potential generation in capsaicin-sensitive primary afferents (Kollarik and Undem, 2004), which results in pain sensation (Schmelz et al, 2000) and release of neuropeptides, such as substance P, that are essential for the development of inflammatory hyperalgesia and hyperreflexia (Ahluwalia et al, 1994;Lecci et al, 1994a,b;Laird et al, 2000;Hunt and Mantyh, 2001).…”

Section: Introductionmentioning

confidence: 99%

Anandamide-Evoked Activation of Vanilloid Receptor 1 Contributes to the Development of Bladder Hyperreflexia and Nociceptive Transmission to Spinal Dorsal Horn Neurons in Cystitis

Dinis¹,

Charrua²,

Avelino³

et al. 2004

J. Neurosci.

182

132

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The role of anandamide in the development of inflammatory hyperalgesia and visceral hyperreflexia was studied in the rat urinary bladder. Animals were given intraperitoneal cyclophosphamide injection, which evokes painful hemorrhagic cystitis accompanied by increased bladder reflex activity. These results suggest that anandamide, through activating TRPV1, contributes to the development of hyperreflexia and hyperalgesia during cystitis.

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“…There is ample evidence that NK1Rs in dorsal horn neurons contribute to the development of hyperalgesia and central sensitization. For example, NK1R antagonists block hyperalgesia (Traub, 1996;Henry et al, 1999), and hyperalgesic responses are absent in transgenic mice lacking the NK1R (De Felipe et al, 1998;Laird et al, 2000; or after selective elimination of dorsal horn neurons possessing NK1Rs .…”

Section: Introductionmentioning

confidence: 99%

Effect of peptidases on the ability of exogenous and endogenous neurokinins to produce neurokinin 1 receptor internalization in the rat spinal cord

Marvizón¹,

Wang

Lao³

et al. 2003

British J Pharmacology

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1 The ability of peptidases to restrict neurokinin 1 receptor (NK1R) activation by exogenously applied or endogenously released neurokinins was investigated by measuring NK1R internalization in rat spinal cord slices. 2 Concentration -response curves for substance P and neurokinin A were obtained in the presence and absence of 10 mM thiorphan, an inhibitor of neutral endopeptidase (EC 3.4.24.11), plus 10 mM captopril, an inhibitor of dipeptidyl carboxypeptidase (EC 3.4.15.1). These inhibitors significantly decreased the EC 50 of substance P to produce NK1R internalization from 32 to 9 nM, and the EC 50 of neurokinin A from 170 to 60 nM. 3 Substance P was significantly more potent than neurokinin A, both with and without these peptidase inhibitors. 4 In the presence of peptidase inhibitors, neurokinin B was 10 times less potent than neurokinin A and 64 times less potent than substance P (EC 50 ¼ 573 nM). 5 Several aminopeptidase inhibitors (actinonin, amastatin, bacitracin, bestatin and puromycin) failed to further increase the effect of thiorphan plus captopril on the NK1R internalization produced by 10 nM substance P. 6 Electrical stimulation of the dorsal root produced NK1R internalization by releasing endogenous neurokinins. Thiorphan plus captopril increased NK1R internalization produced by 1 Hz stimulation, but not by 30 Hz stimulation. 7 Therefore, NEN and DCP restrict NK1R activation by endogenous neurokinins when they are gradually released by low-frequency firing of primary afferents, but become saturated or inhibited when primary afferents fire at a high frequency.

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Deficits in visceral pain and hyperalgesia of mice with a disruption of the tachykinin NK1 receptor gene

Cited by 183 publications

References 42 publications

N-Arachidonoyl Dopamine Modulates Acute Systemic Inflammation via Nonhematopoietic TRPV1

N-Arachidonoyl Dopamine Modulates Acute Systemic Inflammation via Nonhematopoietic TRPV1

Anandamide-Evoked Activation of Vanilloid Receptor 1 Contributes to the Development of Bladder Hyperreflexia and Nociceptive Transmission to Spinal Dorsal Horn Neurons in Cystitis

Effect of peptidases on the ability of exogenous and endogenous neurokinins to produce neurokinin 1 receptor internalization in the rat spinal cord

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