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Effect of lipid raft disruption on TRPV1 receptor activation of trigeminal sensory neurons and transfected cell line.
Eur J Pharmacol. 2010 Feb 25; 628(1-3):67-74.EJ

Abstract

The transient receptor potential vanilloid 1 (TRPV1) is a noxious heat-sensitive, chemonociceptive cation channel which is expressed in primary sensory neurons of polymodal nociceptors. The present study is devoted to analyse the role of lipid raft constituents in calcium influx evoked by various TRPV1 agonists on sensory neurons and on rTRPV1-transfected CHO cell line. Depletion of cholesterol by methyl beta-cyclodextrin (MCD, 1-10mM) diminished the percent of the calcium uptake response of cultured trigeminal neurons to capsaicin (100nM) or resiniferatoxin (RTX, 3nM). In contrast, in TRPV1-transfected cells the inhibition was observed only when capsaicin or N-oleoyldopamine (OLDA, 10microM) was applied, but not when RTX, anandamide (AEA, 10microM) or pH 5.5 was used for gating. The magnitude of Ca(2+)-transients evoked by capsaicin (330nM) was also inhibited in both cell types. Treatment of rTRPV1-expressing cells with sphinomyelinase inhibited the capsaicin-evoked (45)Ca-uptake leaving the RTX-induced response unchanged. On the other hand, in trigeminal neurons the effect of both compounds was inhibited by sphingomyelinase treatment. Inhibition of ganglioside biosynthesis by d-threo-1-Phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP, 10-20microM) or myriocyn (5-50nM) diminished similarly capsaicin- or RTX-evoked calcium uptake in both cultured trigeminal neurons and rTRPV1-expressing cells. The present study revealed that depletion of different constituents of lipid raft inhibited gating the TRPV1 cation channel by various vanilloid and non-vanilloid agents. Evidence for a supporting role of cholesterol, sphingomyelin and gangliosides were obtained both in native and TRPV1-transfected cells. Differential modulation of responses to capsaicin and RTX was often observed.

Authors+Show Affiliations

Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Pécs, Pécs, Hungary. eva.szoke@aok.pte.huNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19958765

Citation

Szoke, Eva, et al. "Effect of Lipid Raft Disruption On TRPV1 Receptor Activation of Trigeminal Sensory Neurons and Transfected Cell Line." European Journal of Pharmacology, vol. 628, no. 1-3, 2010, pp. 67-74.
Szoke E, Börzsei R, Tóth DM, et al. Effect of lipid raft disruption on TRPV1 receptor activation of trigeminal sensory neurons and transfected cell line. Eur J Pharmacol. 2010;628(1-3):67-74.
Szoke, E., Börzsei, R., Tóth, D. M., Lengl, O., Helyes, Z., Sándor, Z., & Szolcsányi, J. (2010). Effect of lipid raft disruption on TRPV1 receptor activation of trigeminal sensory neurons and transfected cell line. European Journal of Pharmacology, 628(1-3), 67-74. https://doi.org/10.1016/j.ejphar.2009.11.052
Szoke E, et al. Effect of Lipid Raft Disruption On TRPV1 Receptor Activation of Trigeminal Sensory Neurons and Transfected Cell Line. Eur J Pharmacol. 2010 Feb 25;628(1-3):67-74. PubMed PMID: 19958765.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of lipid raft disruption on TRPV1 receptor activation of trigeminal sensory neurons and transfected cell line. AU - Szoke,Eva, AU - Börzsei,Rita, AU - Tóth,Dániel Márton, AU - Lengl,Orsolya, AU - Helyes,Zsuzsanna, AU - Sándor,Zoltán, AU - Szolcsányi,János, Y1 - 2009/12/01/ PY - 2009/06/03/received PY - 2009/11/17/revised PY - 2009/11/24/accepted PY - 2009/12/5/entrez PY - 2009/12/5/pubmed PY - 2010/4/7/medline SP - 67 EP - 74 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 628 IS - 1-3 N2 - The transient receptor potential vanilloid 1 (TRPV1) is a noxious heat-sensitive, chemonociceptive cation channel which is expressed in primary sensory neurons of polymodal nociceptors. The present study is devoted to analyse the role of lipid raft constituents in calcium influx evoked by various TRPV1 agonists on sensory neurons and on rTRPV1-transfected CHO cell line. Depletion of cholesterol by methyl beta-cyclodextrin (MCD, 1-10mM) diminished the percent of the calcium uptake response of cultured trigeminal neurons to capsaicin (100nM) or resiniferatoxin (RTX, 3nM). In contrast, in TRPV1-transfected cells the inhibition was observed only when capsaicin or N-oleoyldopamine (OLDA, 10microM) was applied, but not when RTX, anandamide (AEA, 10microM) or pH 5.5 was used for gating. The magnitude of Ca(2+)-transients evoked by capsaicin (330nM) was also inhibited in both cell types. Treatment of rTRPV1-expressing cells with sphinomyelinase inhibited the capsaicin-evoked (45)Ca-uptake leaving the RTX-induced response unchanged. On the other hand, in trigeminal neurons the effect of both compounds was inhibited by sphingomyelinase treatment. Inhibition of ganglioside biosynthesis by d-threo-1-Phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP, 10-20microM) or myriocyn (5-50nM) diminished similarly capsaicin- or RTX-evoked calcium uptake in both cultured trigeminal neurons and rTRPV1-expressing cells. The present study revealed that depletion of different constituents of lipid raft inhibited gating the TRPV1 cation channel by various vanilloid and non-vanilloid agents. Evidence for a supporting role of cholesterol, sphingomyelin and gangliosides were obtained both in native and TRPV1-transfected cells. Differential modulation of responses to capsaicin and RTX was often observed. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/19958765/Effect_of_lipid_raft_disruption_on_TRPV1_receptor_activation_of_trigeminal_sensory_neurons_and_transfected_cell_line_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(09)01104-2 DB - PRIME DP - Unbound Medicine ER -