Effect of NMDA receptor antagonists on protein kinase activated by chronic morphine treatment.

Makimura, Mizue; Iwai, Miho; Sugimoto, Hideya; Fukuda, Hideomi

doi:10.2131/jts.22.57

Cited by 3 publications

(2 citation statements)

References 17 publications

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“…MK-801 inhibited the development of tolerance, as reflected in analgesia, and prevented the increase in protein kinase C, demonstrating a nice correlation between changes in behavior and neurochemistry. Additional studies have explored cellular changes in the spinal cord (Wong et al 1996;Le Guen et al 1999), which may have relevance to tolerance to the analgesic effect of opiates, as well as specific brain regions (Trujillo et al 1991;Garcia and Harlan 1993;Makimura et al 1996Makimura et al , 1997Su et al 1998), which may have relevance to other aspects of opiate tolerance, sensitization or physical dependence (Table 4). Together, these studies demonstrate 1) that the development of opiate tolerance, sensitization and physical dependence are accompanied by cellular changes in the brain and spinal cord that may reflect the neural plasticity underlying the behavioral changes, and 2) that these cellular changes can be inhibited by NMDA receptor antagonists in a manner that parallels the behavioral changes.…”

Section: Discussionmentioning

confidence: 99%

“…The most notable study with regard to the present discussion is that of Bhargava and Matwyshyn (1993), in which they examined the effects of MK-801 on tolerance to the analgesic and the hyperthermic actions of morphine. Whereas MK-801 inhibited tolerance to morphine analgesia, it had no effect on tolerance to morphine-induced hyperthermia, revealing an apparent dissociation between these mor- Trujillo et al (1991) MK-801 Non-comp Rat Morphine-induced increase in striatal prodynorphin peptides (tolerance) Garcia and Harlan (1993) MK-801 Non-comp Rat Morphine-induced increase in striatal calbindin D28 k (tolerance) Mao et al (1995b) MK-801 Non-comp Rat Morphine-induced translocation of protein kinase Cγ in spinal cord (tolerance) Makimura et al (1996) MK-801 Non-comp Rat Withdrawal-induced increase in norepinephrine release in hippocampus (dependence) Wong et al (1996) MK-801 Non-comp Rat Chronic morphine-induced reduction D-AP5 Comp in high-affinity DAMGO binding in spinal cord (tolerance) Makimura et al (1997) MK-801 Non-comp Rat Chronic morphine-induced increase in protein kinase A D-AP5…”

Section: Discussionmentioning

confidence: 99%

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Are NMDA receptors involved in opiate-induced neural and behavioral plasticity?

2000

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NMDA receptor antagonists appear to inhibit the neural plasticity underlying some forms of opiate tolerance, sensitization and physical dependence, suggesting that NMDA receptors are involved in the development of these drug-induced changes in behavior. Further research will help to determine the neural mechanisms responsible for these phenomena, and the therapeutic potential for drugs acting on the NMDA receptor complex in the treatment of pain and addiction.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Are NMDA receptors involved in opiate-induced neural and behavioral plasticity?

2000

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The neurobiology of opiate tolerance, dependence and sensitization: Mechanisms of NMDA receptor-dependent synaptic plasticity

Trujillo

2002

neurotox res

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Long-term administration of opiates leads to changes in the effects of these drugs, including tolerance, sensitization and physical dependence. There is, as yet, incomplete understanding of the neural mechanisms that underlie these phenomena. Tolerance, sensitization and physical dependence can be considered adaptive processes similar to other experience-dependent changes in the brain, such as learning and neural development. There is considerable evidence demonstrating that N-methyl-D-aspartate (NMDA) receptors and downstream signaling cascades may have an important role in different forms of experience-dependent changes in the brain and behavior. This review will explore evidence indicating that NMDA receptors and downstream messengers may be involved in opiate tolerance, sensitization and physical dependence. This evidence has been used to develop a cellular model of NMDA receptor/opiate interactions. According to this model, mu opioid receptor stimulation leads to a protein kinase C-mediated activation of NMDA receptors. Activation of NMDA receptors leads to influx of calcium and activation of calcium-dependent processes. These calcium-dependent processes have the ability to produce critical changes in opioid-responsive neurons, including inhibition of opioid receptor/second messenger coupling. This model is similar to cellular models of learning and neural development in which NMDA receptors have a central role. Together, the evidence suggests that the mechanisms that underlie changes in the brain and behavior produced by long-term opiate use may be similar to other central nervous system adaptations. The experimental findings and the resulting model may have implications for the treatment of pain and addiction.

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Modification of the Expression of Naloxone-Precipitated Withdrawal Signs in Morphine-Dependent Mice by Diabetes: Possible Involvement of Protein Kinase C

Ohsawa

Kamei

1999

Japanese Journal of Pharmacology

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The involvement of cyclic AMP-dependent protein kinase (PKA) and protein kinase C (PKC) in the modulation of naloxone-precipitated withdrawal jumping in morphine-dependent mice by diabetes was examined. Naloxone-precipitated withdrawal jumps were significantly less in morphine-dependent diabetic mice than in morphine-dependent non-diabetic mice. I.c.v. pretreatment with either calphostin C, a PKC inhibitor, or KT-5720, a PKA inhibitor, attenuated naloxone-precipitated withdrawal jumps in morphine-dependent non-diabetic mice. However, naloxone-precipitated withdrawal jumps in morphine-dependent diabetic mice were not attenuated by i.c.v. pretreatment with either calphostin C or KT5720. Moreover, i.c.v. pretreatment with phorbol-12,13-dibutyrate (PDBu), a PKC activator, attenuated naloxone-precipitated withdrawal jumps in morphine-dependent non-diabetic mice, but not in morphine-dependent diabetic mice. The noradrenaline (NA) turnover in the frontal cortex in morphine-dependent non-diabetic mice, but not in morphine-dependent diabetic mice, was significantly increased 5 min after administration of naloxone. Naloxone-induced enhancement of NA turnover in morphine-dependent non-diabetic mice, but not in morphine-dependent diabetic mice, was blocked by i.c.v. pretreatment with either calphostin C or KT5720 1 hr before naloxone challenge and blocked by PDBu 1 hr before the last injection of morphine. These results suggest that the co-activation of PKC and PKA is needed to elicit naloxone-precipitated withdrawal jumps and enhancement of turnover rate of NA in the frontal cortex in morphine-dependent non-diabetic mice. Furthermore, the attenuation of naloxone-precipitated withdrawal jumps in morphine-dependent diabetic mice may be due, in part, to the desensitization of mu-opioid receptors by the activation of PKC.

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Effect of NMDA receptor antagonists on protein kinase activated by chronic morphine treatment.

Cited by 3 publications

References 17 publications

Are NMDA receptors involved in opiate-induced neural and behavioral plasticity?

Are NMDA receptors involved in opiate-induced neural and behavioral plasticity?

The neurobiology of opiate tolerance, dependence and sensitization: Mechanisms of NMDA receptor-dependent synaptic plasticity

Modification of the Expression of Naloxone-Precipitated Withdrawal Signs in Morphine-Dependent Mice by Diabetes: Possible Involvement of Protein Kinase C

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