Role of protein kinase C in desensitization of spinal δ‐opioid‐mediated antinociception in the mouse

Narita, Minoru; Mizoguchi, Hirokazu; Kampine, John P.; Tseng, Leon F.

doi:10.1111/j.1476-5381.1996.tb15610.x

Cited by 54 publications

(29 citation statements)

References 36 publications

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“…In particular, concomitant activation of PKC by DOPr and BK or DOPr and a 2A receptors led to enhanced peripheral (Rowan et al, 2009) and spinal analgesia by DOPr agonists, respectively. However, together with a greater antinociceptive response to DOPr agonists, PKC activity also increased the development of analgesic tolerance, as indicated by potentiation of spinal antinociception by deltorphin II in animals that also received calphostin C (Narita et al, 1996(Narita et al, , 2000. Although tolerance was associated to DOPr desensitization by the kinase (Narita et al, 1996), PKC's contribution to peripheral analgesia was related to its ability to activate phospholipase A2 (PLA2) (Kennedy et al, 1996).…”

Section: D-opioid Receptors and Phospholipase Signalingmentioning

confidence: 99%

Molecular Pharmacology ofδ-Opioid Receptors

et al. 2016

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Section: D-opioid Receptors and Phospholipase Signalingmentioning

confidence: 99%

Molecular Pharmacology ofδ-Opioid Receptors

et al. 2016

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“…Hence, inhibition of kinases involved in receptor phosphorylation and desensitization should abolish the antiproliferative effects of morphine if the hypothesis of "desensitization-dependent growth inhibition" is true. Indeed, inhibition of PKC activity was shown to attenuate the development of opioid tolerance (Narita et al, 1996;Aley et al, 2000;Narita et al, 2001) and to restrict NMDA-R signaling (Mao et al, 1994(Mao et al, , 1995, which has been proposed to account for morphine-induced cell death in spinal cord neurons (Mao et al, 2002). PKC inhibition also prevents a morphine-induced cell cycle 360 TEGEDER AND GEISSLINGER arrest in breast cancer cells (I. Tegeder, unpublished observations).…”

Section: Is Cell Death Initiated By Receptor Desensitizationmentioning

confidence: 99%

Opioids As Modulators of Cell Death and Survival—Unraveling Mechanisms and Revealing New Indications

2004

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“…PKC activators have been shown to inhibit μ, δ, and κ opioid receptor agonist-stimulated analgesia (55)(56)(57)(58). Chronic use of opioid analgesics increases activity and expression of PKC that correlates with a decrease in analgesia.…”

Section: B the Primary Afferent-spinal Cord Synapsementioning

confidence: 99%

Protein kinase C in pain: Involvement of multiple isoforms

Velázquez

Mohammad

Sweitzer

2007

Pharmacological Research

130

125

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Pain is the primary reason that people seek medical care. At present chronic unremitting pain is the third greatest health problem after heart disease and cancer. Chronic pain is an economic burden in lost wages, lost productivity, medical expenses, legal fees and compensation. Chronic pain is defined as a pain of greater than two months duration and can be of an inflammatory or neuropathic origin that can arise following nerve injury or in the absence of any apparent injury. Chronic pain is characterized by an altered pain perception that includes allodynia (a response to a normally nonnoxious stimuli), and hyperalgesia (an exaggerated response to a normally noxious stimuli). This type of pain is often insensitive to the traditional pain drugs or surgical intervention and thus the study of the cellular and molecular mechanisms that contribute to chronic pain are of the up-most importance for the development of a new generation of analgesic agents. Protein kinase C isozymes are under investigation as potential therapeutics for the treatment of chronic pain conditions. The anatomical localization of protein kinase C isozymes in both peripheral and central nervous system sites that process pain have made them the topic of basic science research for close to two decades. This review will outline the research to date on protein kinase C involvement in pain and analgesia. In addition, this review will try to synthesize these works to begin to develop a comprehensive mechanistic understanding of how protein kinase C may function as the master regulator of peripheral and central sensitization that underlies many chronic pain conditions.

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Role of protein kinase C in desensitization of spinal δ‐opioid‐mediated antinociception in the mouse

Cited by 54 publications

References 36 publications

Molecular Pharmacology ofδ-Opioid Receptors

Molecular Pharmacology ofδ-Opioid Receptors

Opioids As Modulators of Cell Death and Survival—Unraveling Mechanisms and Revealing New Indications

Protein kinase C in pain: Involvement of multiple isoforms

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