Abstract
PnTx4(6-1), henceforth renamed δ-Ctenitoxin-Pn1a (δ-CNTX-Pn1a), a peptide from Phoneutria nigriventer spider venom, initially described as an insect toxin, binds to site 3 of sodium channels in nerve cord synaptosomes and slows down sodium current inactivation in isolated axons in cockroaches (Periplaneta americana). δ-CNTX-Pn1a does not cause any apparent toxicity to mice, when intracerebroventricularly injected (30 μg). In this study, we evaluated the antinociceptive effect of δ-CNTX-Pn1a in three animal pain models and investigated its mechanism of action in acute pain. In the inflammatory pain model, induced by carrageenan, δ-CNTX-Pn1a restored the nociceptive threshold of rats, when intraplantarly injected, 2 h and 30 min after carrageenan administration. Concerning the neuropathic pain model, δ-CNTX-Pn1a, when intrathecally administered, reversed the hyperalgesia evoked by sciatic nerve constriction. In the acute pain model, induced by prostaglandin E2, intrathecal administration of δ-CNTX-Pn1a caused a dose-dependent antinociceptive effect. Using antagonists of the receptors, we showed that the antinociceptive effect of δ-CNTX-Pn1a involves both the cannabinoid system, through CB1 receptors, and the opioid system, through μ and δ receptors. Our data show, for the first time, that δ-Ctenitoxin-Pn1a is able to induce antinociception in inflammatory, neuropathic and acute pain models.
Highlights
The word pain derives from the Latin poena, which means “penalty” [1], and treating pain has always been a challenge to mankind since ancient times
We focused on δ-CNTX-Pn1a, a peptide isolated from the venom of the
33 of antinociception when peripherally tested in rats [38], this work aims at looking for the putative antinociception when peripherally tested in rats [38], this work aims at looking for the putative antinociceptive effect of δ‐CNTX‐Pn1a in different experimental pain models in rats: inflammatory, antinociceptive effect of δ-CNTX-Pn1a in different experimental pain models in rats: inflammatory, neuropathic and nociceptive
Summary
The word pain derives from the Latin poena, which means “penalty” [1], and treating pain has always been a challenge to mankind since ancient times. The International Association for the Study of Pain describes it as “an unpleasant sensory and emotional experience associated with real or potential tissue damage”. Further understanding on the mechanisms by which pain signals are interpreted, transmitted and maintained will improve pain treatment strategies. A number of novel approaches using animal toxins to relieve pain have been investigated [2,3,4,5,6,7]. Peptides derived from animal venoms, including scorpions, spiders, amphibians, snakes and marine organisms, have been explored as antinociceptive agents.
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