Tags

Type your tag names separated by a space and hit enter

Phα1β toxin prevents capsaicin-induced nociceptive behavior and mechanical hypersensitivity without acting on TRPV1 channels.
Neuropharmacology. 2013 Aug; 71:237-46.N

Abstract

Phα1β toxin is a peptide purified from the venom of the armed spider Phoneutria nigriventer, with markedly antinociceptive action in models of acute and persistent pain in rats. Similarly to ziconotide, its analgesic action is related to inhibition of high voltage activated calcium channels with more selectivity for N-type. In this study we evaluated the effect of Phα1β when injected peripherally or intrathecally in a rat model of spontaneous pain induced by capsaicin. We also investigated the effect of Phα1β on Ca²⁺ transients in cultured dorsal root ganglia (DRG) neurons and HEK293 cells expressing the TRPV1 receptor. Intraplantar or intrathecal administered Phα1β reduced both nocifensive behavior and mechanical hypersensitivity induced by capsaicin similarly to that observed with SB366791, a specific TRPV1 antagonist. Peripheral nifedipine and mibefradil did also decrease nociceptive behavior induced by intraplantar capsaicin. In contrast, ω-conotoxin MVIIA (a selective N-type Ca²⁺ channel blocker) was effective only when administered intrathecally. Phα1β, MVIIA and SB366791 inhibited, with similar potency, the capsaicin-induced Ca²⁺ transients in DRG neurons. The simultaneous administration of Phα1β and SB366791 inhibited the capsaicin-induced Ca²⁺ transients that were additive suggesting that they act through different targets. Moreover, Phα1β did not inhibit capsaicin-activated currents in patch-clamp recordings of HEK293 cells that expressed TRPV1 receptors. Our results show that Phα1β may be effective as a therapeutic strategy for pain and this effect is not related to the inhibition of TRPV1 receptors.

Authors+Show Affiliations

Instituto de Ensino e Pesquisa da Santa Casa Belo Horizonte, Rua Domingos Vieira 590, Belo Horizonte, MG, Brazil. celiojcjunior@gmail.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

23597507

Citation

Castro-Junior, Celio J., et al. "Phα1β Toxin Prevents Capsaicin-induced Nociceptive Behavior and Mechanical Hypersensitivity Without Acting On TRPV1 Channels." Neuropharmacology, vol. 71, 2013, pp. 237-46.
Castro-Junior CJ, Milano J, Souza AH, et al. Phα1β toxin prevents capsaicin-induced nociceptive behavior and mechanical hypersensitivity without acting on TRPV1 channels. Neuropharmacology. 2013;71:237-46.
Castro-Junior, C. J., Milano, J., Souza, A. H., Silva, J. F., Rigo, F. K., Dalmolin, G., Cordeiro, M. N., Richardson, M., Barros, A. G., Gomez, R. S., Silva, M. A., Kushmerick, C., Ferreira, J., & Gomez, M. V. (2013). Phα1β toxin prevents capsaicin-induced nociceptive behavior and mechanical hypersensitivity without acting on TRPV1 channels. Neuropharmacology, 71, 237-46. https://doi.org/10.1016/j.neuropharm.2013.04.001
Castro-Junior CJ, et al. Phα1β Toxin Prevents Capsaicin-induced Nociceptive Behavior and Mechanical Hypersensitivity Without Acting On TRPV1 Channels. Neuropharmacology. 2013;71:237-46. PubMed PMID: 23597507.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Phα1β toxin prevents capsaicin-induced nociceptive behavior and mechanical hypersensitivity without acting on TRPV1 channels. AU - Castro-Junior,Celio J, AU - Milano,Julie, AU - Souza,Alessandra H, AU - Silva,Juliana F, AU - Rigo,Flávia K, AU - Dalmolin,Geruza, AU - Cordeiro,Marta N, AU - Richardson,Michael, AU - Barros,Alexandre G A, AU - Gomez,Renato S, AU - Silva,Marco A R, AU - Kushmerick,Christopher, AU - Ferreira,Juliano, AU - Gomez,Marcus V, Y1 - 2013/04/15/ PY - 2012/10/02/received PY - 2013/03/22/revised PY - 2013/04/04/accepted PY - 2013/4/20/entrez PY - 2013/4/20/pubmed PY - 2014/1/11/medline SP - 237 EP - 46 JF - Neuropharmacology JO - Neuropharmacology VL - 71 N2 - Phα1β toxin is a peptide purified from the venom of the armed spider Phoneutria nigriventer, with markedly antinociceptive action in models of acute and persistent pain in rats. Similarly to ziconotide, its analgesic action is related to inhibition of high voltage activated calcium channels with more selectivity for N-type. In this study we evaluated the effect of Phα1β when injected peripherally or intrathecally in a rat model of spontaneous pain induced by capsaicin. We also investigated the effect of Phα1β on Ca²⁺ transients in cultured dorsal root ganglia (DRG) neurons and HEK293 cells expressing the TRPV1 receptor. Intraplantar or intrathecal administered Phα1β reduced both nocifensive behavior and mechanical hypersensitivity induced by capsaicin similarly to that observed with SB366791, a specific TRPV1 antagonist. Peripheral nifedipine and mibefradil did also decrease nociceptive behavior induced by intraplantar capsaicin. In contrast, ω-conotoxin MVIIA (a selective N-type Ca²⁺ channel blocker) was effective only when administered intrathecally. Phα1β, MVIIA and SB366791 inhibited, with similar potency, the capsaicin-induced Ca²⁺ transients in DRG neurons. The simultaneous administration of Phα1β and SB366791 inhibited the capsaicin-induced Ca²⁺ transients that were additive suggesting that they act through different targets. Moreover, Phα1β did not inhibit capsaicin-activated currents in patch-clamp recordings of HEK293 cells that expressed TRPV1 receptors. Our results show that Phα1β may be effective as a therapeutic strategy for pain and this effect is not related to the inhibition of TRPV1 receptors. SN - 1873-7064 UR - https://www.unboundmedicine.com/medline/citation/23597507/Phα1β_toxin_prevents_capsaicin_induced_nociceptive_behavior_and_mechanical_hypersensitivity_without_acting_on_TRPV1_channels_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(13)00138-X DB - PRIME DP - Unbound Medicine ER -