Effects of cannabinoids on capsaicin receptor activity following exposure of primary sensory neurons to inflammatory mediators

Neil D. Soneji, Cleoper C. Paule, Marta Mlynarczyk, I. Nagy

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Aims: Activation of the cannabinoid 1 (CB1) receptor in cultured primary sensory neurons reduces responses mediated through the transient receptor potential vanilloid type 1 receptor (TRPV1), which plays a pivotal role in the development of heat hyperalgesia and visceral hyper-reflexia in inflammatory conditions. Here, we studied the effect of cannabinoid-evoked inhibitory effect on TRPV1 in inflammatory conditions. Main methods: The effect of anandamide (1nM-30nM) and 1,1-dimethylheptyl-11-hydroxytetrahydrocannabinol (HU210; 1μM-10μM) was assessed on capsaicin (10nM or 100nM)-evoked cobalt uptake in rat cultured primary sensory neurons following the incubation of the cells in an "inflammatory environment" created by the major inflammatory mediators, bradykinin (5 μM), prostaglandin E2 (5 μM) and nerve growth factor (100ng/ml) for 10min. Key findings: 1. nM and 10. nM anandamide significantly reduced the 10. nM but not the 100. nM capsaicin-evoked responses. HU210 did not produce a significant change in responses evoked by capsaicin at either of its concentrations. The anandamide-induced inhibitory effect could not be reversed by the CB1 receptor antagonist, rimonabant (200. nM) or the membrane-permeable cAMP analogue, 8Br-cAMP (100. μM). Significance: These findings suggest that anandamide may inhibit TRPV1-mediated responses in a non-CB1/non-cannabinoid 2 receptor-dependent manner in primary sensory neurons in inflammatory conditions.

Original languageEnglish
Pages (from-to)162-168
Number of pages7
JournalLife Sciences
Volume87
Issue number5-6
DOIs
Publication statusPublished - Jul 2010

Fingerprint

TRPV Cation Channels
Cannabinoids
Sensory Receptor Cells
Neurons
Capsaicin
rimonabant
Cannabinoid Receptor Antagonists
Cannabinoid Receptors
Hyperalgesia
Bradykinin
Nerve Growth Factor
Cobalt
Dinoprostone
Rats
Hot Temperature
Chemical activation
Cells
Membranes
anandamide
HU 211

Keywords

  • CB1
  • Nociception
  • Non-CB1/non-CB2
  • Pain
  • Transient receptor potential vanilloid type 1 ion channel
  • TRPV1

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Effects of cannabinoids on capsaicin receptor activity following exposure of primary sensory neurons to inflammatory mediators. / Soneji, Neil D.; Paule, Cleoper C.; Mlynarczyk, Marta; Nagy, I.

In: Life Sciences, Vol. 87, No. 5-6, 07.2010, p. 162-168.

Research output: Contribution to journalArticle

Soneji, Neil D. ; Paule, Cleoper C. ; Mlynarczyk, Marta ; Nagy, I. / Effects of cannabinoids on capsaicin receptor activity following exposure of primary sensory neurons to inflammatory mediators. In: Life Sciences. 2010 ; Vol. 87, No. 5-6. pp. 162-168.
@article{cde6ce94478641d89ab9615e933e3321,
title = "Effects of cannabinoids on capsaicin receptor activity following exposure of primary sensory neurons to inflammatory mediators",
abstract = "Aims: Activation of the cannabinoid 1 (CB1) receptor in cultured primary sensory neurons reduces responses mediated through the transient receptor potential vanilloid type 1 receptor (TRPV1), which plays a pivotal role in the development of heat hyperalgesia and visceral hyper-reflexia in inflammatory conditions. Here, we studied the effect of cannabinoid-evoked inhibitory effect on TRPV1 in inflammatory conditions. Main methods: The effect of anandamide (1nM-30nM) and 1,1-dimethylheptyl-11-hydroxytetrahydrocannabinol (HU210; 1μM-10μM) was assessed on capsaicin (10nM or 100nM)-evoked cobalt uptake in rat cultured primary sensory neurons following the incubation of the cells in an {"}inflammatory environment{"} created by the major inflammatory mediators, bradykinin (5 μM), prostaglandin E2 (5 μM) and nerve growth factor (100ng/ml) for 10min. Key findings: 1. nM and 10. nM anandamide significantly reduced the 10. nM but not the 100. nM capsaicin-evoked responses. HU210 did not produce a significant change in responses evoked by capsaicin at either of its concentrations. The anandamide-induced inhibitory effect could not be reversed by the CB1 receptor antagonist, rimonabant (200. nM) or the membrane-permeable cAMP analogue, 8Br-cAMP (100. μM). Significance: These findings suggest that anandamide may inhibit TRPV1-mediated responses in a non-CB1/non-cannabinoid 2 receptor-dependent manner in primary sensory neurons in inflammatory conditions.",
keywords = "CB1, Nociception, Non-CB1/non-CB2, Pain, Transient receptor potential vanilloid type 1 ion channel, TRPV1",
author = "Soneji, {Neil D.} and Paule, {Cleoper C.} and Marta Mlynarczyk and I. Nagy",
year = "2010",
month = "7",
doi = "10.1016/j.lfs.2010.06.003",
language = "English",
volume = "87",
pages = "162--168",
journal = "Life Sciences",
issn = "0024-3205",
publisher = "Elsevier Inc.",
number = "5-6",

}

TY - JOUR

T1 - Effects of cannabinoids on capsaicin receptor activity following exposure of primary sensory neurons to inflammatory mediators

AU - Soneji, Neil D.

AU - Paule, Cleoper C.

AU - Mlynarczyk, Marta

AU - Nagy, I.

PY - 2010/7

Y1 - 2010/7

N2 - Aims: Activation of the cannabinoid 1 (CB1) receptor in cultured primary sensory neurons reduces responses mediated through the transient receptor potential vanilloid type 1 receptor (TRPV1), which plays a pivotal role in the development of heat hyperalgesia and visceral hyper-reflexia in inflammatory conditions. Here, we studied the effect of cannabinoid-evoked inhibitory effect on TRPV1 in inflammatory conditions. Main methods: The effect of anandamide (1nM-30nM) and 1,1-dimethylheptyl-11-hydroxytetrahydrocannabinol (HU210; 1μM-10μM) was assessed on capsaicin (10nM or 100nM)-evoked cobalt uptake in rat cultured primary sensory neurons following the incubation of the cells in an "inflammatory environment" created by the major inflammatory mediators, bradykinin (5 μM), prostaglandin E2 (5 μM) and nerve growth factor (100ng/ml) for 10min. Key findings: 1. nM and 10. nM anandamide significantly reduced the 10. nM but not the 100. nM capsaicin-evoked responses. HU210 did not produce a significant change in responses evoked by capsaicin at either of its concentrations. The anandamide-induced inhibitory effect could not be reversed by the CB1 receptor antagonist, rimonabant (200. nM) or the membrane-permeable cAMP analogue, 8Br-cAMP (100. μM). Significance: These findings suggest that anandamide may inhibit TRPV1-mediated responses in a non-CB1/non-cannabinoid 2 receptor-dependent manner in primary sensory neurons in inflammatory conditions.

AB - Aims: Activation of the cannabinoid 1 (CB1) receptor in cultured primary sensory neurons reduces responses mediated through the transient receptor potential vanilloid type 1 receptor (TRPV1), which plays a pivotal role in the development of heat hyperalgesia and visceral hyper-reflexia in inflammatory conditions. Here, we studied the effect of cannabinoid-evoked inhibitory effect on TRPV1 in inflammatory conditions. Main methods: The effect of anandamide (1nM-30nM) and 1,1-dimethylheptyl-11-hydroxytetrahydrocannabinol (HU210; 1μM-10μM) was assessed on capsaicin (10nM or 100nM)-evoked cobalt uptake in rat cultured primary sensory neurons following the incubation of the cells in an "inflammatory environment" created by the major inflammatory mediators, bradykinin (5 μM), prostaglandin E2 (5 μM) and nerve growth factor (100ng/ml) for 10min. Key findings: 1. nM and 10. nM anandamide significantly reduced the 10. nM but not the 100. nM capsaicin-evoked responses. HU210 did not produce a significant change in responses evoked by capsaicin at either of its concentrations. The anandamide-induced inhibitory effect could not be reversed by the CB1 receptor antagonist, rimonabant (200. nM) or the membrane-permeable cAMP analogue, 8Br-cAMP (100. μM). Significance: These findings suggest that anandamide may inhibit TRPV1-mediated responses in a non-CB1/non-cannabinoid 2 receptor-dependent manner in primary sensory neurons in inflammatory conditions.

KW - CB1

KW - Nociception

KW - Non-CB1/non-CB2

KW - Pain

KW - Transient receptor potential vanilloid type 1 ion channel

KW - TRPV1

UR - http://www.scopus.com/inward/record.url?scp=77954952865&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77954952865&partnerID=8YFLogxK

U2 - 10.1016/j.lfs.2010.06.003

DO - 10.1016/j.lfs.2010.06.003

M3 - Article

C2 - 20598325

AN - SCOPUS:77954952865

VL - 87

SP - 162

EP - 168

JO - Life Sciences

JF - Life Sciences

SN - 0024-3205

IS - 5-6

ER -