Isozyme-specific effects of protein kinase C in pain modulation

Chengshui Zhao, Michael Leitges, Robert W. Gereau

Research output: Contribution to journalArticle

Abstract

BACKGROUND: Protein kinase C (PKC) is a family of serine/threonine kinases that contains more than 10 isozymes. Evidence suggests that PKC may play important roles in pain modulation, but the isozyme-specific effects of PKC on different aspects of pain modulation are not fully understood. We hypothesize that different PKC isozymes play different roles in different aspects of pain modulation. METHODS: The nociceptive behaviors of mice with deletion of PKCα, β, γ, or δ in multiple pain models were compared with their respective wild-type littermates. Also, morphine analgesia and the development of morphine tolerance in mice with deletion of PKCγ were compared with their respective wild-type littermates. RESULTS: Thermal hyperalgesia induced by complete Freund's adjuvant injection was significantly attenuated by the deletion of PKCβ, γ, or δ, but not PKCα. Deletion of PKCγ significantly attenuated neuropathic mechanical allodynia induced by spared nerve injury, whereas deletion of PKCα enhanced this allodynia. Baseline thermal and mechanical sensitivity, nociceptive behaviors induced by formalin, mechanical allodynia induced by complete Freund's adjuvant injection, were not altered by deletion of PKCα, β, γ, or δ. Finally, morphine analgesia and the development of morphine tolerance were not altered in PKCγ-deficient mice. CONCLUSIONS: PKC has isozyme-specific effects in pain modulation.

Original languageEnglish (US)
Pages (from-to)1261-1270
Number of pages10
JournalAnesthesiology
Volume115
Issue number6
DOIs
StatePublished - Dec 1 2011
Externally publishedYes

Fingerprint

Protein Kinase C
Isoenzymes
Pain
Hyperalgesia
Morphine
Freund's Adjuvant
Analgesia
Injections
Protein-Serine-Threonine Kinases
Formaldehyde
Hot Temperature

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Isozyme-specific effects of protein kinase C in pain modulation. / Zhao, Chengshui; Leitges, Michael; Gereau, Robert W.

In: Anesthesiology, Vol. 115, No. 6, 01.12.2011, p. 1261-1270.

Research output: Contribution to journalArticle

Zhao, Chengshui ; Leitges, Michael ; Gereau, Robert W. / Isozyme-specific effects of protein kinase C in pain modulation. In: Anesthesiology. 2011 ; Vol. 115, No. 6. pp. 1261-1270.
@article{68a8f0fc78fe4825bbc579cefb92c4e0,
title = "Isozyme-specific effects of protein kinase C in pain modulation",
abstract = "BACKGROUND: Protein kinase C (PKC) is a family of serine/threonine kinases that contains more than 10 isozymes. Evidence suggests that PKC may play important roles in pain modulation, but the isozyme-specific effects of PKC on different aspects of pain modulation are not fully understood. We hypothesize that different PKC isozymes play different roles in different aspects of pain modulation. METHODS: The nociceptive behaviors of mice with deletion of PKCα, β, γ, or δ in multiple pain models were compared with their respective wild-type littermates. Also, morphine analgesia and the development of morphine tolerance in mice with deletion of PKCγ were compared with their respective wild-type littermates. RESULTS: Thermal hyperalgesia induced by complete Freund's adjuvant injection was significantly attenuated by the deletion of PKCβ, γ, or δ, but not PKCα. Deletion of PKCγ significantly attenuated neuropathic mechanical allodynia induced by spared nerve injury, whereas deletion of PKCα enhanced this allodynia. Baseline thermal and mechanical sensitivity, nociceptive behaviors induced by formalin, mechanical allodynia induced by complete Freund's adjuvant injection, were not altered by deletion of PKCα, β, γ, or δ. Finally, morphine analgesia and the development of morphine tolerance were not altered in PKCγ-deficient mice. CONCLUSIONS: PKC has isozyme-specific effects in pain modulation.",
author = "Chengshui Zhao and Michael Leitges and Gereau, {Robert W.}",
year = "2011",
month = "12",
day = "1",
doi = "10.1097/ALN.0b013e3182390788",
language = "English (US)",
volume = "115",
pages = "1261--1270",
journal = "Anesthesiology",
issn = "0003-3022",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - Isozyme-specific effects of protein kinase C in pain modulation

AU - Zhao, Chengshui

AU - Leitges, Michael

AU - Gereau, Robert W.

PY - 2011/12/1

Y1 - 2011/12/1

N2 - BACKGROUND: Protein kinase C (PKC) is a family of serine/threonine kinases that contains more than 10 isozymes. Evidence suggests that PKC may play important roles in pain modulation, but the isozyme-specific effects of PKC on different aspects of pain modulation are not fully understood. We hypothesize that different PKC isozymes play different roles in different aspects of pain modulation. METHODS: The nociceptive behaviors of mice with deletion of PKCα, β, γ, or δ in multiple pain models were compared with their respective wild-type littermates. Also, morphine analgesia and the development of morphine tolerance in mice with deletion of PKCγ were compared with their respective wild-type littermates. RESULTS: Thermal hyperalgesia induced by complete Freund's adjuvant injection was significantly attenuated by the deletion of PKCβ, γ, or δ, but not PKCα. Deletion of PKCγ significantly attenuated neuropathic mechanical allodynia induced by spared nerve injury, whereas deletion of PKCα enhanced this allodynia. Baseline thermal and mechanical sensitivity, nociceptive behaviors induced by formalin, mechanical allodynia induced by complete Freund's adjuvant injection, were not altered by deletion of PKCα, β, γ, or δ. Finally, morphine analgesia and the development of morphine tolerance were not altered in PKCγ-deficient mice. CONCLUSIONS: PKC has isozyme-specific effects in pain modulation.

AB - BACKGROUND: Protein kinase C (PKC) is a family of serine/threonine kinases that contains more than 10 isozymes. Evidence suggests that PKC may play important roles in pain modulation, but the isozyme-specific effects of PKC on different aspects of pain modulation are not fully understood. We hypothesize that different PKC isozymes play different roles in different aspects of pain modulation. METHODS: The nociceptive behaviors of mice with deletion of PKCα, β, γ, or δ in multiple pain models were compared with their respective wild-type littermates. Also, morphine analgesia and the development of morphine tolerance in mice with deletion of PKCγ were compared with their respective wild-type littermates. RESULTS: Thermal hyperalgesia induced by complete Freund's adjuvant injection was significantly attenuated by the deletion of PKCβ, γ, or δ, but not PKCα. Deletion of PKCγ significantly attenuated neuropathic mechanical allodynia induced by spared nerve injury, whereas deletion of PKCα enhanced this allodynia. Baseline thermal and mechanical sensitivity, nociceptive behaviors induced by formalin, mechanical allodynia induced by complete Freund's adjuvant injection, were not altered by deletion of PKCα, β, γ, or δ. Finally, morphine analgesia and the development of morphine tolerance were not altered in PKCγ-deficient mice. CONCLUSIONS: PKC has isozyme-specific effects in pain modulation.

UR - http://www.scopus.com/inward/record.url?scp=81855167079&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=81855167079&partnerID=8YFLogxK

U2 - 10.1097/ALN.0b013e3182390788

DO - 10.1097/ALN.0b013e3182390788

M3 - Article

C2 - 22042410

AN - SCOPUS:81855167079

VL - 115

SP - 1261

EP - 1270

JO - Anesthesiology

JF - Anesthesiology

SN - 0003-3022

IS - 6

ER -