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A. Brack - One of the best experts on this subject based on the ideXlab platform.
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antinociception by neutrophil derived Opioid peptides in noninflamed tissue role of hypertonicity and the perineurium
Brain Behavior and Immunity, 2009Co-Authors: Heike L Rittner, Dagmar Hackel, Shaaban A Mousa, Michael Schafer, Christoph Stein, Reine-solange Yamdeu, A. BrackAbstract:Abstract Inflammatory pain can be controlled by intraplantar Opioid injection or by secretion of endogenous Opioid peptides from leukocytes in inflamed rat paws. Antinociception requires binding of Opioid peptides to Opioid receptors on peripheral sensory nerve terminals. In the absence of inflammation, hydrophilic Opioid peptides do not penetrate the perineurial barrier and, thus, do not elicit antinociception. This study was designed to examine the conditions under which endogenous, neutrophil-derived hydrophilic Opioid peptides (i.e. Met-Enkephalin and β-endorphin) can raise nociceptive thresholds in noninflamed tissue in rats. Intraplantar injection of the chemokine CXCL2/3 (macrophage inflammatory protein-2) induced selective neutrophil recruitment without overt signs of inflammation or changes in mechanical nociceptive thresholds (paw pressure threshold). Following intraplantar injection of hypertonic saline, the perineurial barrier was permeable for hours and intraplantar injection of Opioid peptides increased mechanical nociceptive thresholds. While formyl-Met-Leu-Phe (fMLP) triggered Opioid peptide release from neutrophils in vitro , nociceptive thresholds were unchanged in vivo . In vitro, hypertonicity interfered with fMLP-induced p38 mitogen activated kinase (MAPK) phosphorylation and Opioid peptide release from neutrophils. These inhibitory effects were fully reversible by washout . In vivo , return to normotonicity occurred within 30 min while the perineurium remained permeable for hours. Under these conditions, fMLP triggered MAPK phosphorylation and induced Opioid peptide-mediated increases in nociceptive thresholds in the noninflamed paw. Taken together, antinociception mediated by endogenous Opioids in noninflamed tissue has two important requirements: (i) opening of the perineurial barrier for Opioid peptide access and (ii) Opioid peptide release from neutrophils involving p38 MAPK.
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Antinociception by neutrophil-derived Opioid peptides in noninflamed tissue—Role of hypertonicity and the perineurium
Brain Behavior and Immunity, 2009Co-Authors: Heike L Rittner, Dagmar Hackel, Shaaban A Mousa, Michael Schafer, Christoph Stein, Reine-solange Yamdeu, A. BrackAbstract:Abstract Inflammatory pain can be controlled by intraplantar Opioid injection or by secretion of endogenous Opioid peptides from leukocytes in inflamed rat paws. Antinociception requires binding of Opioid peptides to Opioid receptors on peripheral sensory nerve terminals. In the absence of inflammation, hydrophilic Opioid peptides do not penetrate the perineurial barrier and, thus, do not elicit antinociception. This study was designed to examine the conditions under which endogenous, neutrophil-derived hydrophilic Opioid peptides (i.e. Met-Enkephalin and β-endorphin) can raise nociceptive thresholds in noninflamed tissue in rats. Intraplantar injection of the chemokine CXCL2/3 (macrophage inflammatory protein-2) induced selective neutrophil recruitment without overt signs of inflammation or changes in mechanical nociceptive thresholds (paw pressure threshold). Following intraplantar injection of hypertonic saline, the perineurial barrier was permeable for hours and intraplantar injection of Opioid peptides increased mechanical nociceptive thresholds. While formyl-Met-Leu-Phe (fMLP) triggered Opioid peptide release from neutrophils in vitro , nociceptive thresholds were unchanged in vivo . In vitro, hypertonicity interfered with fMLP-induced p38 mitogen activated kinase (MAPK) phosphorylation and Opioid peptide release from neutrophils. These inhibitory effects were fully reversible by washout . In vivo , return to normotonicity occurred within 30 min while the perineurium remained permeable for hours. Under these conditions, fMLP triggered MAPK phosphorylation and induced Opioid peptide-mediated increases in nociceptive thresholds in the noninflamed paw. Taken together, antinociception mediated by endogenous Opioids in noninflamed tissue has two important requirements: (i) opening of the perineurial barrier for Opioid peptide access and (ii) Opioid peptide release from neutrophils involving p38 MAPK.
Heike L Rittner - One of the best experts on this subject based on the ideXlab platform.
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antinociception by neutrophil derived Opioid peptides in noninflamed tissue role of hypertonicity and the perineurium
Brain Behavior and Immunity, 2009Co-Authors: Heike L Rittner, Dagmar Hackel, Shaaban A Mousa, Michael Schafer, Christoph Stein, Reine-solange Yamdeu, A. BrackAbstract:Abstract Inflammatory pain can be controlled by intraplantar Opioid injection or by secretion of endogenous Opioid peptides from leukocytes in inflamed rat paws. Antinociception requires binding of Opioid peptides to Opioid receptors on peripheral sensory nerve terminals. In the absence of inflammation, hydrophilic Opioid peptides do not penetrate the perineurial barrier and, thus, do not elicit antinociception. This study was designed to examine the conditions under which endogenous, neutrophil-derived hydrophilic Opioid peptides (i.e. Met-Enkephalin and β-endorphin) can raise nociceptive thresholds in noninflamed tissue in rats. Intraplantar injection of the chemokine CXCL2/3 (macrophage inflammatory protein-2) induced selective neutrophil recruitment without overt signs of inflammation or changes in mechanical nociceptive thresholds (paw pressure threshold). Following intraplantar injection of hypertonic saline, the perineurial barrier was permeable for hours and intraplantar injection of Opioid peptides increased mechanical nociceptive thresholds. While formyl-Met-Leu-Phe (fMLP) triggered Opioid peptide release from neutrophils in vitro , nociceptive thresholds were unchanged in vivo . In vitro, hypertonicity interfered with fMLP-induced p38 mitogen activated kinase (MAPK) phosphorylation and Opioid peptide release from neutrophils. These inhibitory effects were fully reversible by washout . In vivo , return to normotonicity occurred within 30 min while the perineurium remained permeable for hours. Under these conditions, fMLP triggered MAPK phosphorylation and induced Opioid peptide-mediated increases in nociceptive thresholds in the noninflamed paw. Taken together, antinociception mediated by endogenous Opioids in noninflamed tissue has two important requirements: (i) opening of the perineurial barrier for Opioid peptide access and (ii) Opioid peptide release from neutrophils involving p38 MAPK.
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Antinociception by neutrophil-derived Opioid peptides in noninflamed tissue—Role of hypertonicity and the perineurium
Brain Behavior and Immunity, 2009Co-Authors: Heike L Rittner, Dagmar Hackel, Shaaban A Mousa, Michael Schafer, Christoph Stein, Reine-solange Yamdeu, A. BrackAbstract:Abstract Inflammatory pain can be controlled by intraplantar Opioid injection or by secretion of endogenous Opioid peptides from leukocytes in inflamed rat paws. Antinociception requires binding of Opioid peptides to Opioid receptors on peripheral sensory nerve terminals. In the absence of inflammation, hydrophilic Opioid peptides do not penetrate the perineurial barrier and, thus, do not elicit antinociception. This study was designed to examine the conditions under which endogenous, neutrophil-derived hydrophilic Opioid peptides (i.e. Met-Enkephalin and β-endorphin) can raise nociceptive thresholds in noninflamed tissue in rats. Intraplantar injection of the chemokine CXCL2/3 (macrophage inflammatory protein-2) induced selective neutrophil recruitment without overt signs of inflammation or changes in mechanical nociceptive thresholds (paw pressure threshold). Following intraplantar injection of hypertonic saline, the perineurial barrier was permeable for hours and intraplantar injection of Opioid peptides increased mechanical nociceptive thresholds. While formyl-Met-Leu-Phe (fMLP) triggered Opioid peptide release from neutrophils in vitro , nociceptive thresholds were unchanged in vivo . In vitro, hypertonicity interfered with fMLP-induced p38 mitogen activated kinase (MAPK) phosphorylation and Opioid peptide release from neutrophils. These inhibitory effects were fully reversible by washout . In vivo , return to normotonicity occurred within 30 min while the perineurium remained permeable for hours. Under these conditions, fMLP triggered MAPK phosphorylation and induced Opioid peptide-mediated increases in nociceptive thresholds in the noninflamed paw. Taken together, antinociception mediated by endogenous Opioids in noninflamed tissue has two important requirements: (i) opening of the perineurial barrier for Opioid peptide access and (ii) Opioid peptide release from neutrophils involving p38 MAPK.
Christoph Stein - One of the best experts on this subject based on the ideXlab platform.
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antinociception by neutrophil derived Opioid peptides in noninflamed tissue role of hypertonicity and the perineurium
Brain Behavior and Immunity, 2009Co-Authors: Heike L Rittner, Dagmar Hackel, Shaaban A Mousa, Michael Schafer, Christoph Stein, Reine-solange Yamdeu, A. BrackAbstract:Abstract Inflammatory pain can be controlled by intraplantar Opioid injection or by secretion of endogenous Opioid peptides from leukocytes in inflamed rat paws. Antinociception requires binding of Opioid peptides to Opioid receptors on peripheral sensory nerve terminals. In the absence of inflammation, hydrophilic Opioid peptides do not penetrate the perineurial barrier and, thus, do not elicit antinociception. This study was designed to examine the conditions under which endogenous, neutrophil-derived hydrophilic Opioid peptides (i.e. Met-Enkephalin and β-endorphin) can raise nociceptive thresholds in noninflamed tissue in rats. Intraplantar injection of the chemokine CXCL2/3 (macrophage inflammatory protein-2) induced selective neutrophil recruitment without overt signs of inflammation or changes in mechanical nociceptive thresholds (paw pressure threshold). Following intraplantar injection of hypertonic saline, the perineurial barrier was permeable for hours and intraplantar injection of Opioid peptides increased mechanical nociceptive thresholds. While formyl-Met-Leu-Phe (fMLP) triggered Opioid peptide release from neutrophils in vitro , nociceptive thresholds were unchanged in vivo . In vitro, hypertonicity interfered with fMLP-induced p38 mitogen activated kinase (MAPK) phosphorylation and Opioid peptide release from neutrophils. These inhibitory effects were fully reversible by washout . In vivo , return to normotonicity occurred within 30 min while the perineurium remained permeable for hours. Under these conditions, fMLP triggered MAPK phosphorylation and induced Opioid peptide-mediated increases in nociceptive thresholds in the noninflamed paw. Taken together, antinociception mediated by endogenous Opioids in noninflamed tissue has two important requirements: (i) opening of the perineurial barrier for Opioid peptide access and (ii) Opioid peptide release from neutrophils involving p38 MAPK.
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Antinociception by neutrophil-derived Opioid peptides in noninflamed tissue—Role of hypertonicity and the perineurium
Brain Behavior and Immunity, 2009Co-Authors: Heike L Rittner, Dagmar Hackel, Shaaban A Mousa, Michael Schafer, Christoph Stein, Reine-solange Yamdeu, A. BrackAbstract:Abstract Inflammatory pain can be controlled by intraplantar Opioid injection or by secretion of endogenous Opioid peptides from leukocytes in inflamed rat paws. Antinociception requires binding of Opioid peptides to Opioid receptors on peripheral sensory nerve terminals. In the absence of inflammation, hydrophilic Opioid peptides do not penetrate the perineurial barrier and, thus, do not elicit antinociception. This study was designed to examine the conditions under which endogenous, neutrophil-derived hydrophilic Opioid peptides (i.e. Met-Enkephalin and β-endorphin) can raise nociceptive thresholds in noninflamed tissue in rats. Intraplantar injection of the chemokine CXCL2/3 (macrophage inflammatory protein-2) induced selective neutrophil recruitment without overt signs of inflammation or changes in mechanical nociceptive thresholds (paw pressure threshold). Following intraplantar injection of hypertonic saline, the perineurial barrier was permeable for hours and intraplantar injection of Opioid peptides increased mechanical nociceptive thresholds. While formyl-Met-Leu-Phe (fMLP) triggered Opioid peptide release from neutrophils in vitro , nociceptive thresholds were unchanged in vivo . In vitro, hypertonicity interfered with fMLP-induced p38 mitogen activated kinase (MAPK) phosphorylation and Opioid peptide release from neutrophils. These inhibitory effects were fully reversible by washout . In vivo , return to normotonicity occurred within 30 min while the perineurium remained permeable for hours. Under these conditions, fMLP triggered MAPK phosphorylation and induced Opioid peptide-mediated increases in nociceptive thresholds in the noninflamed paw. Taken together, antinociception mediated by endogenous Opioids in noninflamed tissue has two important requirements: (i) opening of the perineurial barrier for Opioid peptide access and (ii) Opioid peptide release from neutrophils involving p38 MAPK.
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Leukocyte-derived Opioid peptides and inhibition of pain.
Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2006Co-Authors: Halina Machelska, Christoph SteinAbstract:In peripheral inflamed tissue interactions between leukocyte-derived Opioid peptides and Opioid receptors on sensory neurons lead to potent, clinically relevant inhibition of pain. Opioid receptors are present on peripheral terminals of sensory neurons and are upregulated in inflammation. Their endogenous ligands, Opioid peptides, are synthesized in circulating immune cells, which migrate to injured tissues directed by chemokines and adhesion molecules. Under stressful stimuli or in response to releasing agents (e.g., corticotropin-releasing factor, cytokines, catecholamines) leukocytes can secrete Opioids. These peptides activate peripheral Opioid receptors and produce analgesia by inhibiting the excitability of sensory nerves and/or the release of excitatory neuropeptides. These effects occur without central Opioid side effects such as depression of breathing, clouding of consciousness, or addiction. Future research should elucidate the selective targeting of Opioid peptide-containing immune cells to sites of painful tissue injury and the augmentation of Opioid peptide and receptor synthesis.
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local analgesic effect of endogenous Opioid peptides
The Lancet, 1993Co-Authors: Christoph Stein, A H S Hassan, K Lehrberger, J Giefing, Alexander YassouridisAbstract:Opioids produce analgesia by interacting with local Opioid receptors in peripheral inflamed tissue. This study investigated whether endogenous ligands of these receptors are present in synovia and whether such Opioid peptides can inhibit pain by activation of intra-articular Opioid receptors. Samples of synovium from 8 patients undergoing arthroscopic knee surgery were examined by immunohistochemistry for the presence of beta-endorphin, met-enkephalin, and dynorphin. All tissue samples showed synovitis. Inflammatory cells stained strongly for beta-endorphin and met-enkephalin but not for dynorphin. To find out whether blockade of intra-articular Opioid receptors affected pain, we randomly assigned 22 patients undergoing arthroscopic knee surgery to receive naloxone (0.04 mg) intra-articularly (n = 10) or intravenously (n = 12); each patient received a placebo injection into the other site. Postoperative pain was assessed by visual analogue scale, a numerical rating scale, the McGill pain questionnaire, and supplementary analgesic consumption during the next 24 h. All pain scores were higher in the intra-articular naloxone group than in the intravenous naloxone group. The differences were significant (p < 0.05) during the first 4 h. Supplementary analgesic consumption was significantly higher in the intra-articular group (52.5 [14.0] vs 15.6 [8.0] mg diclofenac, p < 0.05). Opioid peptides are present in inflamed synovial tissue and can inhibit pain after knee surgery through an action specific to intra-articular Opioid receptors. These findings expand the gate control theory of pain and suggest new approaches such as the development of peripherally acting Opioid analgesics without central side-effects.
Shaaban A Mousa - One of the best experts on this subject based on the ideXlab platform.
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antinociception by neutrophil derived Opioid peptides in noninflamed tissue role of hypertonicity and the perineurium
Brain Behavior and Immunity, 2009Co-Authors: Heike L Rittner, Dagmar Hackel, Shaaban A Mousa, Michael Schafer, Christoph Stein, Reine-solange Yamdeu, A. BrackAbstract:Abstract Inflammatory pain can be controlled by intraplantar Opioid injection or by secretion of endogenous Opioid peptides from leukocytes in inflamed rat paws. Antinociception requires binding of Opioid peptides to Opioid receptors on peripheral sensory nerve terminals. In the absence of inflammation, hydrophilic Opioid peptides do not penetrate the perineurial barrier and, thus, do not elicit antinociception. This study was designed to examine the conditions under which endogenous, neutrophil-derived hydrophilic Opioid peptides (i.e. Met-Enkephalin and β-endorphin) can raise nociceptive thresholds in noninflamed tissue in rats. Intraplantar injection of the chemokine CXCL2/3 (macrophage inflammatory protein-2) induced selective neutrophil recruitment without overt signs of inflammation or changes in mechanical nociceptive thresholds (paw pressure threshold). Following intraplantar injection of hypertonic saline, the perineurial barrier was permeable for hours and intraplantar injection of Opioid peptides increased mechanical nociceptive thresholds. While formyl-Met-Leu-Phe (fMLP) triggered Opioid peptide release from neutrophils in vitro , nociceptive thresholds were unchanged in vivo . In vitro, hypertonicity interfered with fMLP-induced p38 mitogen activated kinase (MAPK) phosphorylation and Opioid peptide release from neutrophils. These inhibitory effects were fully reversible by washout . In vivo , return to normotonicity occurred within 30 min while the perineurium remained permeable for hours. Under these conditions, fMLP triggered MAPK phosphorylation and induced Opioid peptide-mediated increases in nociceptive thresholds in the noninflamed paw. Taken together, antinociception mediated by endogenous Opioids in noninflamed tissue has two important requirements: (i) opening of the perineurial barrier for Opioid peptide access and (ii) Opioid peptide release from neutrophils involving p38 MAPK.
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Antinociception by neutrophil-derived Opioid peptides in noninflamed tissue—Role of hypertonicity and the perineurium
Brain Behavior and Immunity, 2009Co-Authors: Heike L Rittner, Dagmar Hackel, Shaaban A Mousa, Michael Schafer, Christoph Stein, Reine-solange Yamdeu, A. BrackAbstract:Abstract Inflammatory pain can be controlled by intraplantar Opioid injection or by secretion of endogenous Opioid peptides from leukocytes in inflamed rat paws. Antinociception requires binding of Opioid peptides to Opioid receptors on peripheral sensory nerve terminals. In the absence of inflammation, hydrophilic Opioid peptides do not penetrate the perineurial barrier and, thus, do not elicit antinociception. This study was designed to examine the conditions under which endogenous, neutrophil-derived hydrophilic Opioid peptides (i.e. Met-Enkephalin and β-endorphin) can raise nociceptive thresholds in noninflamed tissue in rats. Intraplantar injection of the chemokine CXCL2/3 (macrophage inflammatory protein-2) induced selective neutrophil recruitment without overt signs of inflammation or changes in mechanical nociceptive thresholds (paw pressure threshold). Following intraplantar injection of hypertonic saline, the perineurial barrier was permeable for hours and intraplantar injection of Opioid peptides increased mechanical nociceptive thresholds. While formyl-Met-Leu-Phe (fMLP) triggered Opioid peptide release from neutrophils in vitro , nociceptive thresholds were unchanged in vivo . In vitro, hypertonicity interfered with fMLP-induced p38 mitogen activated kinase (MAPK) phosphorylation and Opioid peptide release from neutrophils. These inhibitory effects were fully reversible by washout . In vivo , return to normotonicity occurred within 30 min while the perineurium remained permeable for hours. Under these conditions, fMLP triggered MAPK phosphorylation and induced Opioid peptide-mediated increases in nociceptive thresholds in the noninflamed paw. Taken together, antinociception mediated by endogenous Opioids in noninflamed tissue has two important requirements: (i) opening of the perineurial barrier for Opioid peptide access and (ii) Opioid peptide release from neutrophils involving p38 MAPK.
Dagmar Hackel - One of the best experts on this subject based on the ideXlab platform.
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antinociception by neutrophil derived Opioid peptides in noninflamed tissue role of hypertonicity and the perineurium
Brain Behavior and Immunity, 2009Co-Authors: Heike L Rittner, Dagmar Hackel, Shaaban A Mousa, Michael Schafer, Christoph Stein, Reine-solange Yamdeu, A. BrackAbstract:Abstract Inflammatory pain can be controlled by intraplantar Opioid injection or by secretion of endogenous Opioid peptides from leukocytes in inflamed rat paws. Antinociception requires binding of Opioid peptides to Opioid receptors on peripheral sensory nerve terminals. In the absence of inflammation, hydrophilic Opioid peptides do not penetrate the perineurial barrier and, thus, do not elicit antinociception. This study was designed to examine the conditions under which endogenous, neutrophil-derived hydrophilic Opioid peptides (i.e. Met-Enkephalin and β-endorphin) can raise nociceptive thresholds in noninflamed tissue in rats. Intraplantar injection of the chemokine CXCL2/3 (macrophage inflammatory protein-2) induced selective neutrophil recruitment without overt signs of inflammation or changes in mechanical nociceptive thresholds (paw pressure threshold). Following intraplantar injection of hypertonic saline, the perineurial barrier was permeable for hours and intraplantar injection of Opioid peptides increased mechanical nociceptive thresholds. While formyl-Met-Leu-Phe (fMLP) triggered Opioid peptide release from neutrophils in vitro , nociceptive thresholds were unchanged in vivo . In vitro, hypertonicity interfered with fMLP-induced p38 mitogen activated kinase (MAPK) phosphorylation and Opioid peptide release from neutrophils. These inhibitory effects were fully reversible by washout . In vivo , return to normotonicity occurred within 30 min while the perineurium remained permeable for hours. Under these conditions, fMLP triggered MAPK phosphorylation and induced Opioid peptide-mediated increases in nociceptive thresholds in the noninflamed paw. Taken together, antinociception mediated by endogenous Opioids in noninflamed tissue has two important requirements: (i) opening of the perineurial barrier for Opioid peptide access and (ii) Opioid peptide release from neutrophils involving p38 MAPK.
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Antinociception by neutrophil-derived Opioid peptides in noninflamed tissue—Role of hypertonicity and the perineurium
Brain Behavior and Immunity, 2009Co-Authors: Heike L Rittner, Dagmar Hackel, Shaaban A Mousa, Michael Schafer, Christoph Stein, Reine-solange Yamdeu, A. BrackAbstract:Abstract Inflammatory pain can be controlled by intraplantar Opioid injection or by secretion of endogenous Opioid peptides from leukocytes in inflamed rat paws. Antinociception requires binding of Opioid peptides to Opioid receptors on peripheral sensory nerve terminals. In the absence of inflammation, hydrophilic Opioid peptides do not penetrate the perineurial barrier and, thus, do not elicit antinociception. This study was designed to examine the conditions under which endogenous, neutrophil-derived hydrophilic Opioid peptides (i.e. Met-Enkephalin and β-endorphin) can raise nociceptive thresholds in noninflamed tissue in rats. Intraplantar injection of the chemokine CXCL2/3 (macrophage inflammatory protein-2) induced selective neutrophil recruitment without overt signs of inflammation or changes in mechanical nociceptive thresholds (paw pressure threshold). Following intraplantar injection of hypertonic saline, the perineurial barrier was permeable for hours and intraplantar injection of Opioid peptides increased mechanical nociceptive thresholds. While formyl-Met-Leu-Phe (fMLP) triggered Opioid peptide release from neutrophils in vitro , nociceptive thresholds were unchanged in vivo . In vitro, hypertonicity interfered with fMLP-induced p38 mitogen activated kinase (MAPK) phosphorylation and Opioid peptide release from neutrophils. These inhibitory effects were fully reversible by washout . In vivo , return to normotonicity occurred within 30 min while the perineurium remained permeable for hours. Under these conditions, fMLP triggered MAPK phosphorylation and induced Opioid peptide-mediated increases in nociceptive thresholds in the noninflamed paw. Taken together, antinociception mediated by endogenous Opioids in noninflamed tissue has two important requirements: (i) opening of the perineurial barrier for Opioid peptide access and (ii) Opioid peptide release from neutrophils involving p38 MAPK.