Inhibitory effect of the NMDA receptor antagonist, dizocilpine (MK-801), on the development of morphine dependence.

Makimura, Mizue; Sugimoto, Hideya; Shinomiya, Kazufusa; Kabasawa, Yozo; Fukuda, Hideomi

doi:10.2131/jts.21.2_135

Cited by 9 publications

(5 citation statements)

References 14 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%

“…However, evidence similar to that discussed above in the section on opiate tolerance suggests that NMDA receptor antagonists do not act on opiate dependence by blocking associative learning processes. First, several studies have demonstrated that NMDA receptor antagonists will inhibit the development of physical dependence acquired through chronic infusion (Ben-Eliyahu et al 1992;Dunbar and Yaksh 1996;Makimura et al 1996;Manning et al 1996;Gonzalez et al 1997;McLemore et al 1997). …”

Section: Nmda Receptor Antagonists and The Development Of Opiate Physmentioning

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%

Section: Nmda Receptor Antagonists and The Development Of Opiate Physmentioning

confidence: 99%

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

2000

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“…In later work, Koyuncuoglu and colleagues (42) showed that NMDA receptor antagonists such as ketamine and dextromethorphan attenuated the severity of morphine withdrawal symptoms in rats. The role of NMDA receptors in the development of opioid tolerance and dependence has been verified by many other investigators (43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55)(56)(57)(58)(59)(60)(61)(62) who showed that antagonism of NMDA receptors (with competitive and noncompetitive antagonists) attenuates these phenomena. More recently, it has been shown that administration of antagonists to the glycine site of the NMDA receptor attenuates opioid withdrawal symptoms (63)(64)(65).…”

Section: Glutamate and Opioid Tolerance And Dependencementioning

confidence: 76%

Common Mechanisms Underlying Opioid Tolerance and Dependence and Neuropathic Pain: Role of Metabotropic Glutamate Receptors

Fundytus

2000

Pain Research and Management

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It has been suggested that opioid tolerance and dependence share common mechanisms with neuropathic pain. This short review deals with the role of glutamate and glutamate receptors in opioid tolerance and dependence, and neuropathic pain. Particular attention is given to the role of metabotropic glutamate receptors (mGluRs). First, the different types of glutamate receptors, which include N-methyl-D-aspartate, alpha-amino-3-hydroxyl-5-methylisoxazole-4-propionic acid, kainate and mGluRs, are described. Following this, evidence suggesting that these receptors are involved in opioid tolerance and dependence are summarized. At the end of this section, a model that has been previously proposed to explain mechanisms by which mGluRs may be involved in opioid tolerance and dependence are described. Next is a discussion of the evidence suggesting that glutamate receptors are similarly involved in neuropathic pain, and also in opioid sensitivity associated with neuropathic pain. Again, a hypothetical model used to explain mechanisms by which mGluRs may be involved in neuropathic pain is briefly described. The relevance of the data is discussed in terms of some of the clinical implications of the material presented in the article. Mécanismes communs sous-jacents à la tolérance et à la dépendance aux substances opioïdes, ainsi qu'aux douleurs névropathiques : rôle des récepteurs du glutamate métabotropique RÉSUMÉ : La tolérance et la dépendance aux substances opioïdes partageraient des mécanismes communs aux douleurs névropathiques. Il sera question, dans le présent survol, du rôle du glutamate et des ré-cepteurs du glutamate dans la tolérance et la dépendance aux substances opioïdes, ainsi que dans les douleurs névropathiques. Une attention particulière est accordée au rôle des récepteurs du glutamate métabotropique (mGluR). Tout d'abord, on décrit les différents types de récepteur du glutamate, notamment le N-méthyl-D-aspartate, l'alpha-amino-3-hydroxyl-5-méthyl-isoxazole-4-acide proprionique, le kaïnate et les mGluR. Suit un résumé des données selon lesquelles ces récepteurs sont mis en cause dans la tolérance et la dépendance aux substances opioïdes. À la fin de cette partie, on décrit un modèle déjà proposé pour expliquer comment les mGluR pourraient participer à ce phénomène de tolérance et de dépendance. Ensuite, il y a une discussion sur les éléments qui donnent à penser que les récepteurs du glutamate sont également mis en cause dans les douleurs névropathiques ainsi que dans la sensibilité aux substances opioïdes, associée aux douleurs névropathiques. Encore une fois, on fait une brève description du modèle hypothétique utilisé pour expliquer comment les mGluR contribueraient aux douleurs névropathiques. La pertinence des données est ici discutée en fonction de certaines des incidences cliniques du matériel présenté dans l'article.

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“…It has been reported that the chronic morphine exposure results in neuroplasticity, which may utilize the same mechanism of high‐frequency train‐induced LTP (Trujillo & Akil, 1991; Tokuyama et al., 1995; Makimura et al., 1996; Lu et al., 2000). Thus one may assume that there are alterations in N ‐methyl‐ d ‐aspartate (NMDA)–induced processes and Ca 2+ channel activity, which may, under chronic morphine administration, enhance PTZ LTP.…”

Section: Discussionmentioning

confidence: 99%

Morphine dependence increases the response to a brief pentylenetetrazol administration in rat hippocampal CA1 in vitro

et al. 2009

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SUMMARYPurpose: Herein we used electrophysiologic approaches in hippocampal area CA1 to estimate how morphine treatment alters the pentylenetetrazol (PTZ) effects. Methods: Hippocampal slices taken from either control animals or animals made dependent via chronic morphine administration were examined. Changes in the population spike and epileptiform amplitudes were used as indices to quantify the effects of PTZ exposure in the control and morphine-dependent slices. Hippocampal slices taken either from control animals or from animals made dependent upon morphine were exposed to PTZ, either with or without morphine, naloxone, or morphine + naloxone. Results: Morphine dependence increased a PTZinduced long-term potentiation (LTP) of the population spike in CA1 in vitro. This LTP was not found in rats that had spontaneously withdrawn morphine or withdrawn with naloxone in vivo after chronic morphine intake. Morphine or naloxone in vitro blocked the PTZ-induced LTP changes in control and morphine-dependent slices. However, PTZ-induced multiple population spikes (epileptiform activity) in CA1 was not blocked by naloxone. Discussion: It is concluded that dependence on morphine enhances PTZ-induced plastic and epileptic changes in CA1 excitability. We suggest that this model of neuronal activity in dependent slices could present an opportunity for studying the mechanisms underlying the increased likelihood of seizures in morphine users.

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Inhibitory effect of the NMDA receptor antagonist, dizocilpine (MK-801), on the development of morphine dependence.

Cited by 9 publications

References 14 publications

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

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

Common Mechanisms Underlying Opioid Tolerance and Dependence and Neuropathic Pain: Role of Metabotropic Glutamate Receptors

Morphine dependence increases the response to a brief pentylenetetrazol administration in rat hippocampal CA1 in vitro

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