Tachykinin NK1 receptor antagonist co-administration attenuates opioid withdrawal-mediated spinal microglia and astrocyte activation

Prolonged morphine treatment increases pain sensitivity in many patients. Enhanced spinal Substance P release is one of the adaptive changes associated with sustained opioid exposure. In addition to pain transmitting second order neurons, spinal microglia and astrocytes also express functionally act...

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Published inEuropean journal of pharmacology Vol. 684; no. 1-3; pp. 64 - 70
Main Authors Tumati, Suneeta, Largent-Milnes, Tally M., Keresztes, Attila I., Yamamoto, Takashi, Vanderah, Todd W., Roeske, William R., Hruby, Victor J., Varga, Eva V.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 05.06.2012
Subjects
agonists
Analgesics, Opioid - administration & dosage
Analgesics, Opioid - adverse effects
Animals
antagonists
astrocytes
Astrocytes - drug effects
Astrocytes - metabolism
Biomarkers - metabolism
CD11b Antigen - metabolism
Hyperalgesia - chemically induced
Hyperalgesia - drug therapy
Hyperalgesia - metabolism
Hyperalgesia - pathology
Male
Microglia - drug effects
Microglia - metabolism
morphine
Morphine - administration & dosage
Morphine - adverse effects
Nerve Tissue Proteins - metabolism
Neurokinin-1 Receptor Antagonists
neurons
Opioid-induced hyperalgesia
pain
patients
Rats
Rats, Sprague-Dawley
receptors
Spinal Cord - drug effects
Spinal Cord - pathology
Spinal glia
substance P
Substance Withdrawal Syndrome - drug therapy
Substance Withdrawal Syndrome - metabolism
Substance Withdrawal Syndrome - pathology
Tachykinin NK1 receptor
Tachykinin NK1 receptor antagonist
Tryptophan - administration & dosage
Tryptophan - analogs & derivatives
Tryptophan - pharmacology
Tryptophan - therapeutic use
Tumor Necrosis Factor-alpha - metabolism
Up-Regulation - drug effects
Opioid-induced hyperalgesia
Tachykinin NK1 receptor
Tachykinin NK1 receptor antagonist
Spinal glia
Online AccessGet full text

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Abstract Prolonged morphine treatment increases pain sensitivity in many patients. Enhanced spinal Substance P release is one of the adaptive changes associated with sustained opioid exposure. In addition to pain transmitting second order neurons, spinal microglia and astrocytes also express functionally active Tachykinin NK1 (Substance P) receptors. In the present work we investigated the role of glial Tachykinin NK1 receptors in morphine withdrawal-mediated spinal microglia and astrocyte activation. Our data indicate that intrathecal co-administration (6days, twice daily) of a selective Tachykinin NK1 receptor antagonist (N-acetyl-l-tryptophan 3,5-bis(trifluoromethyl)benzylester (L-732,138; 20μg/injection)) attenuates spinal microglia and astrocyte marker and pro-inflammatory mediator immunoreactivity as well as hyperalgesia in withdrawn rats. Furthermore, covalent linkage of the opioid agonist with a Tachykinin NK1 antagonist pharmacophore yielded a bivalent compound that did not augment spinal microglia or astrocyte marker or pro-inflammatory mediator immunoreactivity and did not cause paradoxical pain sensitization upon drug withdrawal. Thus, bivalent opioid/Tachykinin NK1 receptor antagonists may provide a novel paradigm for long-term pain management. [Display omitted]
AbstractList Prolonged morphine treatment increases pain sensitivity in many patients. Enhanced spinal Substance P release is one of the adaptive changes associated with sustained opioid exposure. In addition to pain transmitting second order neurons, spinal microglia and astrocytes also express functionally active Tachykinin NK 1 (Substance P) receptors. In the present work we investigated the role of glial Tachykinin NK 1 receptors in morphine withdrawal-mediated spinal microglia and astrocyte activation. Our data indicate that intrathecal co-administration (6 days, twice daily) of a selective Tachykinin NK 1 receptor antagonist (N-acetyl-l-tryptophan 3,5-bis(trifluoromethyl)benzylester (L-732,138; 20 μg/injection) attenuates spinal microglia and astrocyte marker and pro-inflammatory mediator immunoreactivity as well as hyperalgesia in morphine-withdrawn rats. Furthermore, covalent linkage of the opioid agonist with a Tachykinin NK 1 antagonist pharmacophor yielded a bivalent compound that did not augment spinal microglia or astrocyte marker or pro-inflammatory mediator immunoreactivity and did not cause paradoxical pain sensitization upon drug withdrawal. Thus, bivalent opioid/Tachykinin NK 1 receptor antagonists may provide a novel paradigm for long-term pain management.
Prolonged morphine treatment increases pain sensitivity in many patients. Enhanced spinal Substance P release is one of the adaptive changes associated with sustained opioid exposure. In addition to pain transmitting second order neurons, spinal microglia and astrocytes also express functionally active Tachykinin NK₁ (Substance P) receptors. In the present work we investigated the role of glial Tachykinin NK₁ receptors in morphine withdrawal-mediated spinal microglia and astrocyte activation. Our data indicate that intrathecal co-administration (6 days, twice daily) of a selective Tachykinin NK₁ receptor antagonist (N-acetyl-L-tryptophan 3,5-bis(trifluoromethyl)benzylester (L-732,138; 20 μg/injection)) attenuates spinal microglia and astrocyte marker and pro-inflammatory mediator immunoreactivity as well as hyperalgesia in withdrawn rats. Furthermore, covalent linkage of the opioid agonist with a Tachykinin NK₁ antagonist pharmacophore yielded a bivalent compound that did not augment spinal microglia or astrocyte marker or pro-inflammatory mediator immunoreactivity and did not cause paradoxical pain sensitization upon drug withdrawal. Thus, bivalent opioid/Tachykinin NK₁ receptor antagonists may provide a novel paradigm for long-term pain management.
Prolonged morphine treatment increases pain sensitivity in many patients. Enhanced spinal Substance P release is one of the adaptive changes associated with sustained opioid exposure. In addition to pain transmitting second order neurons, spinal microglia and astrocytes also express functionally active Tachykinin NK1 (Substance P) receptors. In the present work we investigated the role of glial Tachykinin NK1 receptors in morphine withdrawal-mediated spinal microglia and astrocyte activation. Our data indicate that intrathecal co-administration (6days, twice daily) of a selective Tachykinin NK1 receptor antagonist (N-acetyl-l-tryptophan 3,5-bis(trifluoromethyl)benzylester (L-732,138; 20μg/injection)) attenuates spinal microglia and astrocyte marker and pro-inflammatory mediator immunoreactivity as well as hyperalgesia in withdrawn rats. Furthermore, covalent linkage of the opioid agonist with a Tachykinin NK1 antagonist pharmacophore yielded a bivalent compound that did not augment spinal microglia or astrocyte marker or pro-inflammatory mediator immunoreactivity and did not cause paradoxical pain sensitization upon drug withdrawal. Thus, bivalent opioid/Tachykinin NK1 receptor antagonists may provide a novel paradigm for long-term pain management. [Display omitted]
Prolonged morphine treatment increases pain sensitivity in many patients. Enhanced spinal Substance P release is one of the adaptive changes associated with sustained opioid exposure. In addition to pain transmitting second order neurons, spinal microglia and astrocytes also express functionally active Tachykinin NK1 (Substance P) receptors. In the present work we investigated the role of glial Tachykinin NK1 receptors in morphine withdrawal-mediated spinal microglia and astrocyte activation. Our data indicate that intrathecal co-administration (6 days, twice daily) of a selective Tachykinin NK1 receptor antagonist (N-acetyl-l-tryptophan 3,5-bis(trifluoromethyl)benzylester (L-732,138; 20 I14g/injection)) attenuates spinal microglia and astrocyte marker and pro-inflammatory mediator immunoreactivity as well as hyperalgesia in withdrawn rats. Furthermore, covalent linkage of the opioid agonist with a Tachykinin NK1 antagonist pharmacophore yielded a bivalent compound that did not augment spinal microglia or astrocyte marker or pro-inflammatory mediator immunoreactivity and did not cause paradoxical pain sensitization upon drug withdrawal. Thus, bivalent opioid/Tachykinin NK1 receptor antagonists may provide a novel paradigm for long-term pain management.
Prolonged morphine treatment increases pain sensitivity in many patients. Enhanced spinal Substance P release is one of the adaptive changes associated with sustained opioid exposure. In addition to pain transmitting second order neurons, spinal microglia and astrocytes also express functionally active Tachykinin NK₁ (Substance P) receptors. In the present work we investigated the role of glial Tachykinin NK₁ receptors in morphine withdrawal-mediated spinal microglia and astrocyte activation. Our data indicate that intrathecal co-administration (6days, twice daily) of a selective Tachykinin NK₁ receptor antagonist (N-acetyl-l-tryptophan 3,5-bis(trifluoromethyl)benzylester (L-732,138; 20μg/injection)) attenuates spinal microglia and astrocyte marker and pro-inflammatory mediator immunoreactivity as well as hyperalgesia in withdrawn rats. Furthermore, covalent linkage of the opioid agonist with a Tachykinin NK₁ antagonist pharmacophore yielded a bivalent compound that did not augment spinal microglia or astrocyte marker or pro-inflammatory mediator immunoreactivity and did not cause paradoxical pain sensitization upon drug withdrawal. Thus, bivalent opioid/Tachykinin NK₁ receptor antagonists may provide a novel paradigm for long-term pain management.
Author Keresztes, Attila I.
Tumati, Suneeta
Varga, Eva V.
Yamamoto, Takashi
Vanderah, Todd W.
Roeske, William R.
Largent-Milnes, Tally M.
Hruby, Victor J.
AuthorAffiliation c Department of Medicine, The University of Arizona, Tucson, AZ 85724, USA
a Department of Pharmacology, The University of Arizona, Tucson, AZ 85724, USA
d Department of Anesthesiology, The University of Arizona, Tucson, AZ 85724, USA
e The Sarver Heart Center, The University of Arizona, Tucson, AZ 85724, USA
b Department of Chemistry, The University of Arizona, Tucson, AZ 85724, USA
AuthorAffiliation_xml – name: a Department of Pharmacology, The University of Arizona, Tucson, AZ 85724, USA
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– name: c Department of Medicine, The University of Arizona, Tucson, AZ 85724, USA
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  givenname: Eva V.
  surname: Varga
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  email: evarga@email.arizona.edu
  organization: Department of Pharmacology, The University of Arizona, Tucson, AZ 85724, USA
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Keywords Opioid-induced hyperalgesia
Tachykinin NK1 receptor
Tachykinin NK1 receptor antagonist
Spinal glia
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Snippet Prolonged morphine treatment increases pain sensitivity in many patients. Enhanced spinal Substance P release is one of the adaptive changes associated with...
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SubjectTerms agonists
Analgesics, Opioid - administration & dosage
Analgesics, Opioid - adverse effects
Animals
antagonists
astrocytes
Astrocytes - drug effects
Astrocytes - metabolism
Biomarkers - metabolism
CD11b Antigen - metabolism
Hyperalgesia - chemically induced
Hyperalgesia - drug therapy
Hyperalgesia - metabolism
Hyperalgesia - pathology
Male
Microglia - drug effects
Microglia - metabolism
morphine
Morphine - administration & dosage
Morphine - adverse effects
Nerve Tissue Proteins - metabolism
Neurokinin-1 Receptor Antagonists
neurons
Opioid-induced hyperalgesia
pain
patients
Rats
Rats, Sprague-Dawley
receptors
Spinal Cord - drug effects
Spinal Cord - pathology
Spinal glia
substance P
Substance Withdrawal Syndrome - drug therapy
Substance Withdrawal Syndrome - metabolism
Substance Withdrawal Syndrome - pathology
Tachykinin NK1 receptor
Tachykinin NK1 receptor antagonist
Tryptophan - administration & dosage
Tryptophan - analogs & derivatives
Tryptophan - pharmacology
Tryptophan - therapeutic use
Tumor Necrosis Factor-alpha - metabolism
Up-Regulation - drug effects
Title Tachykinin NK1 receptor antagonist co-administration attenuates opioid withdrawal-mediated spinal microglia and astrocyte activation
URI https://dx.doi.org/10.1016/j.ejphar.2012.03.025
https://www.ncbi.nlm.nih.gov/pubmed/22724132
https://search.proquest.com/docview/1399913641
https://pubmed.ncbi.nlm.nih.gov/PMC3565540
Volume 684
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