Capsaicin sensitivity is associated with the expression of the vanilloid (capsaicin) receptor (VR1) mRNA in adult rat sensory ganglia

Helliwell, Rachel J. A.; McLatchie, Linda M.; Clarke, Melanie; Winter, Janet; Bevan, Stuart; McIntyre, Peter

doi:10.1016/s0304-3940(98)00475-3

Cited by 173 publications

(103 citation statements)

References 10 publications

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“…The small/medium-size DRG neurons are considered nociceptive sensory neurons belonging to the slowly conducting, unmyelinated (C) and thinly myelinated (Aδ) fibers, respectively [25,53]. C and Aδ fibers-related neurons express high densities of both TRPV1 [11,13,26] and Ttype Ca 2+ channels [54,55,59]. We found that the T-type channels of DRG neurons can be effectively downregulated by the large quantity of Ca 2+ entering the cells during TRPV1 stimulation and facilitated by the possible co-localization of these two channel entities in membrane nano-microdomains.…”

Section: Discussionmentioning

confidence: 99%

Calcium-dependent inhibition of T-type calcium channels by TRPV1 activation in rat sensory neurons

Comunanza

Carbone

Marcantoni

et al. 2011

Pflugers Arch - Eur J Physiol

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We studied the inhibitory effects of transient receptor potential vanilloid-1 (TRPV1) activation by capsaicin on low-voltage-activated (LVA, T-type) Ca 2+ channel and highvoltage-activated (HVA; L, N, P/Q, R) currents in rat DRG sensory neurons, as a potential mechanism underlying capsaicin-induced analgesia. T-type and HVA currents were elicited in whole-cell clamped DRG neurons using ramp commands applied before and after 30-s exposures to 1 μM capsaicin. T-type currents were estimated at the first peak of the I-V characteristics and HVA at the second peak, occurring at more positive potentials. Small and medium-sized DRG neurons responded to capsaicin producing transient inward currents of variable amplitudes, mainly carried by Ca 2+. In those cells responding to capsaicin with a large Ca 2+ influx (59% of the total), a marked inhibition of both T-type and HVA Ca 2+ currents was observed. The percentage of T-type and HVA channel inhibition was prevented by replacing Ca 2+ with Ba 2+ during capsaicin application or applying high doses of intracellular BAPTA (20 mM), suggesting that TRPV1-mediated inhibition of T-type and HVA channels is Ca 2+ -dependent and likely confined to membrane nanomicrodomains. Our data are consistent with the idea that TRPV1-induced analgesia may derive from indirect inhibition of both T-type and HVA channels which, in turn, would reduce the threshold of nociceptive signals generation (T-type channel inhibition) and nociceptive synaptic transmission (HVA-channels inhibition).

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Section: Discussionmentioning

confidence: 99%

Calcium-dependent inhibition of T-type calcium channels by TRPV1 activation in rat sensory neurons

Comunanza

Carbone

Marcantoni

et al. 2011

Pflugers Arch - Eur J Physiol

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“…TRPV1 is highly expressed in the peripheral nervous system, specifically in a subset of small-diameter primary sensory neurons in trigeminal nerve and dorsal root ganglia that detect noxious stimuli and in the inferior (nodose) ganglion of the vagus nerve (9)(10)(11)(12)(13). The peripheral terminals of TRPV1-expressing nociceptors innervate most organs and tissues.…”

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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“…VR1 and P2X3 receptors appear not to be limited to a nociceptive distribution, because they also localize to visceral afferent neurons that send axons via cranial nerves to the brain stem (Helliwell et al, 1998;Tominaga et al, 1998;Mezey et al, 2000). Cranial afferents such as those in nodose ganglion transduce conditions within heart, blood vessels, lungs, and other visceral organs.…”

Section: Introductionmentioning

confidence: 99%

Purinergic and Vanilloid Receptor Activation Releases Glutamate from Separate Cranial Afferent Terminals in Nucleus Tractus Solitarius

Jin¹,

Bailey²,

Li³

et al. 2004

J. Neurosci.

164

162

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Capsaicin sensitivity is associated with the expression of the vanilloid (capsaicin) receptor (VR1) mRNA in adult rat sensory ganglia

Cited by 173 publications

References 10 publications

Calcium-dependent inhibition of T-type calcium channels by TRPV1 activation in rat sensory neurons

Calcium-dependent inhibition of T-type calcium channels by TRPV1 activation in rat sensory neurons

N-Arachidonoyl Dopamine Modulates Acute Systemic Inflammation via Nonhematopoietic TRPV1

Purinergic and Vanilloid Receptor Activation Releases Glutamate from Separate Cranial Afferent Terminals in Nucleus Tractus Solitarius

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