Tail Flick Test

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Esperanza Del Pozo - One of the best experts on this subject based on the ideXlab platform.

  • inhibitors of serine threonine protein phosphatases antagonize the antinociception induced by agonists of α2 adrenoceptors and gabab but not κ opioid receptors in the Tail Flick Test in mice
    Pain, 2005
    Co-Authors: Ana Moncada, Cruz Miguel Cendan, Jose M Baeyens, Esperanza Del Pozo
    Abstract:

    We previously reported that serine/threonine protein phosphatases (PPs) play a role in the antinociception induced by the m-opioid receptor agonist morphine. In this study we evaluated the possible involvement of PPs on the antinociception induced by agonists of others G proteincoupled receptors in the Tail Flick Test in mice. The subcutaneous administration of clonidine (0.25‐4 mg/kg), baclofen (2‐32 mg/kg) or U50,488H (2‐16 mg/kg) (agonists of a2 adrenoceptors, GABAB and k-opioid receptors, respectively) produced dose-dependent antinociception. The antinociceptive effects of clonidine and baclofen were antagonized in a dose-dependent way by the protein phosphatase inhibitors okadaic acid (0.001‐10 pg/mouse, i.c.v.) and cantharidin (0.001‐10 ng/mouse, i.c.v.), and okadaic acid was 1000 times more potent than cantharidin in producing this effect. The effects of these drugs appear to be specifically due to the blockade of PPs, since L-norokadaone (an analogue of okadaic acid that has no effect on PPs) did not modify clonidine- or baclofen-induced antinociception over the wide range of doses used (0.001‐1000 pg/mouse, i.c.v.). On the other hand, the antinociception induced by activation of k-opioid receptors with U50,488H was not modified by okadaic acid or cantharidin. In conclusion, our data support the idea that serine/threonine PPs are differentially involved in the antinociceptive effects of several agonists of G protein-coupled receptors in mice. q 2004 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

  • effects of serine threonine protein phosphatase inhibitors on morphine induced antinociception in the Tail Flick Test in mice
    European Journal of Pharmacology, 2003
    Co-Authors: Ana Moncada, Cruz Miguel Cendan, Jose M Baeyens, Esperanza Del Pozo
    Abstract:

    The aim of this study was to evaluate the effects of serine/threonine protein phosphatase (PP) inhibitors on morphine-induced antinociception in the Tail Flick Test in mice, and on [3H]naloxone binding to the forebrain crude synaptosome fraction. Neither okadaic acid nor cantharidin (1-10000 nM) displaced [3H]naloxone from its specific binding sites, which indicates that they do not interact at the opioid receptor level. The i.c.v. administration of very low doses of okadaic acid (0.001-1 pg/mouse) and cantharidin (0.001-1 ng/mouse), which inhibit PP2A, produced a dose-dependent antagonism of the antinociception induced by morphine (s.c.). However, L-nor-okadaone (0.001 pg/mouse-1 ng/mouse, i.c.v.), an analogue of okadaic acid lacking activity against protein phosphatases, did not affect the antinociceptive effect of morphine. On the other hand, high doses of okadaic acid (10 ng/mouse, i.c.v.) and cantharidin (1 microg/mouse, i.c.v.), which also block PP1, and calyculin-A (0.1 fg/mouse-1 ng/mouse, i.c.v.), which inhibits equally both PP1 and PP2A, did not modify the morphine-induced antinociception. These results suggest that the activation of type 2A serine/threonine protein phosphatases may play a role in the antinociceptive effect of morphine, and that PP1 might counterbalace this activity.

Marcus Vinicius Gomez - One of the best experts on this subject based on the ideXlab platform.

  • antinociceptive effect of brazilian armed spider venom toxin tx3 3 in animal models of neuropathic pain
    Pain, 2011
    Co-Authors: Gerusa Duarte Dalmolin, Cassia Regina Silva, Flavia Karine Rigo, Guilherme M Gomes, Marta N Cordeiro, Michael K Richardson, Marco Aurelio Romano Silva, Marco A M Prado, Marcus Vinicius Gomez
    Abstract:

    Abstract Venoms peptides have produced exceptional sources for drug development to treat pain. In this study we examined the antinociceptive and side effects of Tx3-3, a peptide toxin isolated from Phoneutria nigriventer venom, which inhibits high-voltage-dependent calcium channels (VDCC), preferentially P/Q and R-type VDCC. We Tested the effects of Tx3-3 in animal models of nociceptive (Tail-Flick Test), neuropathic (partial sciatic nerve ligation and streptozotocin-induced diabetic neuropathy), and inflammatory (intraplantar complete Freund’s adjuvant) pain. In the Tail-Flick Test, both intrathecal (i.t.) and intracerebroventricular (i.c.v.) injection of Tx3-3 in mice caused a short-lasting effect (ED 50 and 95% confidence intervals of 8.8 [4.1–18.8] and 3.7 [1.6–8.4] pmol/site for i.t. and i.c.v. injection, respectively), without impairing motor functions, at least at doses 10–30 times higher than the effective dose. By comparison, ω-conotoxin MVIIC, a P/Q and N-type VDCC blocker derived from Conus magus venom, caused significant motor impairment at doses close to efficacious dose in Tail Flick Test. Tx3-3 showed a long-lasting antinociceptive effect in neuropathic pain models. Intrathecal injection of Tx3-3 (30 pmol/site) decreased both mechanical allodynia produced by sciatic nerve injury in mice and streptozotocin-induced allodynia in mice and rats. On the other hand, i.t. injection of Tx3-3 did not alter inflammatory pain. Taken together, our data show that Tx3-3 shows prevalent antinociceptive effects in the neuropathic pain models and does not cause adverse motor effects at antinociceptive efficacious doses, suggesting that this peptide toxin holds promise as a novel therapeutic agent for the control of neuropathic pain.

  • antinociceptive effect of brazilian armed spider venom toxin tx3 3 in animal models of neuropathic pain
    Pain, 2011
    Co-Authors: Gerusa Duarte Dalmolin, Cassia Regina Silva, Flavia Karine Rigo, Guilherme M Gomes, Marta N Cordeiro, Michael K Richardson, Marco Aurelio Romano Silva, Marco A M Prado, Marcus Vinicius Gomez
    Abstract:

    Venoms peptides have produced exceptional sources for drug development to treat pain. In this study we examined the antinociceptive and side effects of Tx3-3, a peptide toxin isolated from Phoneutria nigriventer venom, which inhibits high-voltage-dependent calcium channels (VDCC), preferentially P/Q and R-type VDCC. We Tested the effects of Tx3-3 in animal models of nociceptive (Tail-Flick Test), neuropathic (partial sciatic nerve ligation and streptozotocin-induced diabetic neuropathy), and inflammatory (intraplantar complete Freund's adjuvant) pain. In the Tail-Flick Test, both intrathecal (i.t.) and intracerebroventricular (i.c.v.) injection of Tx3-3 in mice caused a short-lasting effect (ED(50) and 95% confidence intervals of 8.8 [4.1-18.8] and 3.7 [1.6-8.4] pmol/site for i.t. and i.c.v. injection, respectively), without impairing motor functions, at least at doses 10-30 times higher than the effective dose. By comparison, ω-conotoxin MVIIC, a P/Q and N-type VDCC blocker derived from Conus magus venom, caused significant motor impairment at doses close to efficacious dose in Tail Flick Test. Tx3-3 showed a long-lasting antinociceptive effect in neuropathic pain models. Intrathecal injection of Tx3-3 (30 pmol/site) decreased both mechanical allodynia produced by sciatic nerve injury in mice and streptozotocin-induced allodynia in mice and rats. On the other hand, i.t. injection of Tx3-3 did not alter inflammatory pain. Taken together, our data show that Tx3-3 shows prevalent antinociceptive effects in the neuropathic pain models and does not cause adverse motor effects at antinociceptive efficacious doses, suggesting that this peptide toxin holds promise as a novel therapeutic agent for the control of neuropathic pain. The Brazilian armed spider Tx3-3, a new P/Q and R-type calcium channel blocker, effectively alleviates allodynia in animal neuropathic pain models.

Marco A M Prado - One of the best experts on this subject based on the ideXlab platform.

  • antinociceptive effect of brazilian armed spider venom toxin tx3 3 in animal models of neuropathic pain
    Pain, 2011
    Co-Authors: Gerusa Duarte Dalmolin, Cassia Regina Silva, Flavia Karine Rigo, Guilherme M Gomes, Marta N Cordeiro, Michael K Richardson, Marco Aurelio Romano Silva, Marco A M Prado, Marcus Vinicius Gomez
    Abstract:

    Abstract Venoms peptides have produced exceptional sources for drug development to treat pain. In this study we examined the antinociceptive and side effects of Tx3-3, a peptide toxin isolated from Phoneutria nigriventer venom, which inhibits high-voltage-dependent calcium channels (VDCC), preferentially P/Q and R-type VDCC. We Tested the effects of Tx3-3 in animal models of nociceptive (Tail-Flick Test), neuropathic (partial sciatic nerve ligation and streptozotocin-induced diabetic neuropathy), and inflammatory (intraplantar complete Freund’s adjuvant) pain. In the Tail-Flick Test, both intrathecal (i.t.) and intracerebroventricular (i.c.v.) injection of Tx3-3 in mice caused a short-lasting effect (ED 50 and 95% confidence intervals of 8.8 [4.1–18.8] and 3.7 [1.6–8.4] pmol/site for i.t. and i.c.v. injection, respectively), without impairing motor functions, at least at doses 10–30 times higher than the effective dose. By comparison, ω-conotoxin MVIIC, a P/Q and N-type VDCC blocker derived from Conus magus venom, caused significant motor impairment at doses close to efficacious dose in Tail Flick Test. Tx3-3 showed a long-lasting antinociceptive effect in neuropathic pain models. Intrathecal injection of Tx3-3 (30 pmol/site) decreased both mechanical allodynia produced by sciatic nerve injury in mice and streptozotocin-induced allodynia in mice and rats. On the other hand, i.t. injection of Tx3-3 did not alter inflammatory pain. Taken together, our data show that Tx3-3 shows prevalent antinociceptive effects in the neuropathic pain models and does not cause adverse motor effects at antinociceptive efficacious doses, suggesting that this peptide toxin holds promise as a novel therapeutic agent for the control of neuropathic pain.

  • antinociceptive effect of brazilian armed spider venom toxin tx3 3 in animal models of neuropathic pain
    Pain, 2011
    Co-Authors: Gerusa Duarte Dalmolin, Cassia Regina Silva, Flavia Karine Rigo, Guilherme M Gomes, Marta N Cordeiro, Michael K Richardson, Marco Aurelio Romano Silva, Marco A M Prado, Marcus Vinicius Gomez
    Abstract:

    Venoms peptides have produced exceptional sources for drug development to treat pain. In this study we examined the antinociceptive and side effects of Tx3-3, a peptide toxin isolated from Phoneutria nigriventer venom, which inhibits high-voltage-dependent calcium channels (VDCC), preferentially P/Q and R-type VDCC. We Tested the effects of Tx3-3 in animal models of nociceptive (Tail-Flick Test), neuropathic (partial sciatic nerve ligation and streptozotocin-induced diabetic neuropathy), and inflammatory (intraplantar complete Freund's adjuvant) pain. In the Tail-Flick Test, both intrathecal (i.t.) and intracerebroventricular (i.c.v.) injection of Tx3-3 in mice caused a short-lasting effect (ED(50) and 95% confidence intervals of 8.8 [4.1-18.8] and 3.7 [1.6-8.4] pmol/site for i.t. and i.c.v. injection, respectively), without impairing motor functions, at least at doses 10-30 times higher than the effective dose. By comparison, ω-conotoxin MVIIC, a P/Q and N-type VDCC blocker derived from Conus magus venom, caused significant motor impairment at doses close to efficacious dose in Tail Flick Test. Tx3-3 showed a long-lasting antinociceptive effect in neuropathic pain models. Intrathecal injection of Tx3-3 (30 pmol/site) decreased both mechanical allodynia produced by sciatic nerve injury in mice and streptozotocin-induced allodynia in mice and rats. On the other hand, i.t. injection of Tx3-3 did not alter inflammatory pain. Taken together, our data show that Tx3-3 shows prevalent antinociceptive effects in the neuropathic pain models and does not cause adverse motor effects at antinociceptive efficacious doses, suggesting that this peptide toxin holds promise as a novel therapeutic agent for the control of neuropathic pain. The Brazilian armed spider Tx3-3, a new P/Q and R-type calcium channel blocker, effectively alleviates allodynia in animal neuropathic pain models.

Ana Moncada - One of the best experts on this subject based on the ideXlab platform.

  • inhibitors of serine threonine protein phosphatases antagonize the antinociception induced by agonists of α2 adrenoceptors and gabab but not κ opioid receptors in the Tail Flick Test in mice
    Pain, 2005
    Co-Authors: Ana Moncada, Cruz Miguel Cendan, Jose M Baeyens, Esperanza Del Pozo
    Abstract:

    We previously reported that serine/threonine protein phosphatases (PPs) play a role in the antinociception induced by the m-opioid receptor agonist morphine. In this study we evaluated the possible involvement of PPs on the antinociception induced by agonists of others G proteincoupled receptors in the Tail Flick Test in mice. The subcutaneous administration of clonidine (0.25‐4 mg/kg), baclofen (2‐32 mg/kg) or U50,488H (2‐16 mg/kg) (agonists of a2 adrenoceptors, GABAB and k-opioid receptors, respectively) produced dose-dependent antinociception. The antinociceptive effects of clonidine and baclofen were antagonized in a dose-dependent way by the protein phosphatase inhibitors okadaic acid (0.001‐10 pg/mouse, i.c.v.) and cantharidin (0.001‐10 ng/mouse, i.c.v.), and okadaic acid was 1000 times more potent than cantharidin in producing this effect. The effects of these drugs appear to be specifically due to the blockade of PPs, since L-norokadaone (an analogue of okadaic acid that has no effect on PPs) did not modify clonidine- or baclofen-induced antinociception over the wide range of doses used (0.001‐1000 pg/mouse, i.c.v.). On the other hand, the antinociception induced by activation of k-opioid receptors with U50,488H was not modified by okadaic acid or cantharidin. In conclusion, our data support the idea that serine/threonine PPs are differentially involved in the antinociceptive effects of several agonists of G protein-coupled receptors in mice. q 2004 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

  • effects of serine threonine protein phosphatase inhibitors on morphine induced antinociception in the Tail Flick Test in mice
    European Journal of Pharmacology, 2003
    Co-Authors: Ana Moncada, Cruz Miguel Cendan, Jose M Baeyens, Esperanza Del Pozo
    Abstract:

    The aim of this study was to evaluate the effects of serine/threonine protein phosphatase (PP) inhibitors on morphine-induced antinociception in the Tail Flick Test in mice, and on [3H]naloxone binding to the forebrain crude synaptosome fraction. Neither okadaic acid nor cantharidin (1-10000 nM) displaced [3H]naloxone from its specific binding sites, which indicates that they do not interact at the opioid receptor level. The i.c.v. administration of very low doses of okadaic acid (0.001-1 pg/mouse) and cantharidin (0.001-1 ng/mouse), which inhibit PP2A, produced a dose-dependent antagonism of the antinociception induced by morphine (s.c.). However, L-nor-okadaone (0.001 pg/mouse-1 ng/mouse, i.c.v.), an analogue of okadaic acid lacking activity against protein phosphatases, did not affect the antinociceptive effect of morphine. On the other hand, high doses of okadaic acid (10 ng/mouse, i.c.v.) and cantharidin (1 microg/mouse, i.c.v.), which also block PP1, and calyculin-A (0.1 fg/mouse-1 ng/mouse, i.c.v.), which inhibits equally both PP1 and PP2A, did not modify the morphine-induced antinociception. These results suggest that the activation of type 2A serine/threonine protein phosphatases may play a role in the antinociceptive effect of morphine, and that PP1 might counterbalace this activity.

Gerusa Duarte Dalmolin - One of the best experts on this subject based on the ideXlab platform.

  • antinociceptive effect of brazilian armed spider venom toxin tx3 3 in animal models of neuropathic pain
    Pain, 2011
    Co-Authors: Gerusa Duarte Dalmolin, Cassia Regina Silva, Flavia Karine Rigo, Guilherme M Gomes, Marta N Cordeiro, Michael K Richardson, Marco Aurelio Romano Silva, Marco A M Prado, Marcus Vinicius Gomez
    Abstract:

    Abstract Venoms peptides have produced exceptional sources for drug development to treat pain. In this study we examined the antinociceptive and side effects of Tx3-3, a peptide toxin isolated from Phoneutria nigriventer venom, which inhibits high-voltage-dependent calcium channels (VDCC), preferentially P/Q and R-type VDCC. We Tested the effects of Tx3-3 in animal models of nociceptive (Tail-Flick Test), neuropathic (partial sciatic nerve ligation and streptozotocin-induced diabetic neuropathy), and inflammatory (intraplantar complete Freund’s adjuvant) pain. In the Tail-Flick Test, both intrathecal (i.t.) and intracerebroventricular (i.c.v.) injection of Tx3-3 in mice caused a short-lasting effect (ED 50 and 95% confidence intervals of 8.8 [4.1–18.8] and 3.7 [1.6–8.4] pmol/site for i.t. and i.c.v. injection, respectively), without impairing motor functions, at least at doses 10–30 times higher than the effective dose. By comparison, ω-conotoxin MVIIC, a P/Q and N-type VDCC blocker derived from Conus magus venom, caused significant motor impairment at doses close to efficacious dose in Tail Flick Test. Tx3-3 showed a long-lasting antinociceptive effect in neuropathic pain models. Intrathecal injection of Tx3-3 (30 pmol/site) decreased both mechanical allodynia produced by sciatic nerve injury in mice and streptozotocin-induced allodynia in mice and rats. On the other hand, i.t. injection of Tx3-3 did not alter inflammatory pain. Taken together, our data show that Tx3-3 shows prevalent antinociceptive effects in the neuropathic pain models and does not cause adverse motor effects at antinociceptive efficacious doses, suggesting that this peptide toxin holds promise as a novel therapeutic agent for the control of neuropathic pain.

  • antinociceptive effect of brazilian armed spider venom toxin tx3 3 in animal models of neuropathic pain
    Pain, 2011
    Co-Authors: Gerusa Duarte Dalmolin, Cassia Regina Silva, Flavia Karine Rigo, Guilherme M Gomes, Marta N Cordeiro, Michael K Richardson, Marco Aurelio Romano Silva, Marco A M Prado, Marcus Vinicius Gomez
    Abstract:

    Venoms peptides have produced exceptional sources for drug development to treat pain. In this study we examined the antinociceptive and side effects of Tx3-3, a peptide toxin isolated from Phoneutria nigriventer venom, which inhibits high-voltage-dependent calcium channels (VDCC), preferentially P/Q and R-type VDCC. We Tested the effects of Tx3-3 in animal models of nociceptive (Tail-Flick Test), neuropathic (partial sciatic nerve ligation and streptozotocin-induced diabetic neuropathy), and inflammatory (intraplantar complete Freund's adjuvant) pain. In the Tail-Flick Test, both intrathecal (i.t.) and intracerebroventricular (i.c.v.) injection of Tx3-3 in mice caused a short-lasting effect (ED(50) and 95% confidence intervals of 8.8 [4.1-18.8] and 3.7 [1.6-8.4] pmol/site for i.t. and i.c.v. injection, respectively), without impairing motor functions, at least at doses 10-30 times higher than the effective dose. By comparison, ω-conotoxin MVIIC, a P/Q and N-type VDCC blocker derived from Conus magus venom, caused significant motor impairment at doses close to efficacious dose in Tail Flick Test. Tx3-3 showed a long-lasting antinociceptive effect in neuropathic pain models. Intrathecal injection of Tx3-3 (30 pmol/site) decreased both mechanical allodynia produced by sciatic nerve injury in mice and streptozotocin-induced allodynia in mice and rats. On the other hand, i.t. injection of Tx3-3 did not alter inflammatory pain. Taken together, our data show that Tx3-3 shows prevalent antinociceptive effects in the neuropathic pain models and does not cause adverse motor effects at antinociceptive efficacious doses, suggesting that this peptide toxin holds promise as a novel therapeutic agent for the control of neuropathic pain. The Brazilian armed spider Tx3-3, a new P/Q and R-type calcium channel blocker, effectively alleviates allodynia in animal neuropathic pain models.