N-methyl-D-aspartate receptors involved in morphine-induced hyperalgesia in sensitized mice

Ahmadi, Shamseddin; Golbaghi, Hajar; Azizbeigi, Ronak; Esmailzadeh, Nabaz

doi:10.1016/j.ejphar.2014.04.048

Cited by 18 publications

(9 citation statements)

References 44 publications

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“…Consistent with prior reports of this association, the regimen of repeated morphine treatment used in this study produced both an enhancement of acid-stimulated stretching and tolerance to the decrease in acid-stimulated stretching produced by 1.0 mg/kg morphine. This is consistent with previous publications showing tolerance to morphine antinociception in assays of acid-stimulated stretching in rats (Fernandes et al, 1977; Feng et al, 1994) and mice (Su et al, 2000), and it also agrees with evidence for morphine antinociceptive tolerance in other assays of pain-stimulated behavior, such as tail-flick and hot-plate procedures (Dong et al, 2006; Lilius et al, 2009; Lin et al, 2011; Ahmadi et al, 2014). However, dissociations between opioid-induced hyperalgesia and tolerance have also been reported in both preclinical and clinical studies (Juni et al, 2006; Chu et al, 2012), and the present results in the assay of acid-depressed ICSS provide another example of this dissociation.…”

Section: Discussionsupporting

confidence: 93%

Differential tolerance to morphine antinociception in assays of pain-stimulated vs. pain-depressed behavior in rats

Altarifi

Negus

2015

European Journal of Pharmacology

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In preclinical research on pain and analgesia, noxious stimuli can stimulate expression of some behaviors (e.g. withdrawal reflexes) and depress others (e.g. feeding, locomotion, and positively reinforced operant responding). Tolerance to morphine antinociception is a robust and reliable phenomenon in preclinical assays of pain-stimulated behavior, but development of morphine tolerance in assays of pain-depressed behavior has not been studied. This study compared morphine antinociceptive tolerance in parallel assays of pain-stimulated and pain-depressed behavior in male Sprague-Dawley rats. Intraperitoneal injection of dilute lactic acid served as a noxious stimulus to stimulate a stretching response in one group of rats and to depress operant responding for electrical brain stimulation (intracranial self-stimulation; ICSS) in another group of rats. Antinociception produced by morphine (1.0 mg/kg) was determined after a regimen of chronic treatment with either saline or morphine in separate subgroups of rats in each procedure. In rats receiving chronic saline, acid alone stimulated a stretching response and depressed ICSS, and both acid effects were blocked by 1.0 mg/kg morphine. Rats receiving chronic morphine displayed hyperalgesic responses to the acid noxious stimulus in both procedures. Complete tolerance developed to morphine antinociception in the assay of acid-stimulated stretching, but morphine retained full antinociceptive effectiveness in the assay of acid-depressed ICSS. These results suggest that morphine antinociception in an assay of pain-depressed behavior is relatively resistant to tolerance. More broadly, these results suggest that antinociceptive tolerance can develop at different rates or to different degrees for different measures of antinociception.

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Section: Discussionsupporting

confidence: 93%

Differential tolerance to morphine antinociception in assays of pain-stimulated vs. pain-depressed behavior in rats

Altarifi

Negus

2015

European Journal of Pharmacology

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“…In our previous study, we showed that the hypernociceptive behavior observed in adult rats using the formalin test after morphine exposure during early life could be related to stimulation of NMDA pathway because NMDA antagonist (ketamine) administration totally reversed the effects of morphine (Rozisky et al, 2011). Additionally, Ahmadi et al (2014) showed that co‐administration of D‐(−)‐2‐amino‐5‐phosphonopentanoic acid (D‐AP5), a competitive NMDA receptor antagonist, or magnesium sulfate (MgSO 4 ), a NMDA receptor channel blocker, in mice presensitized by morphine, significantly prevented the decrease in analgesic effect of morphine at higher doses (10 and 15 mg/kg). Furthermore, low doses of morphine (1 μg/kg) can trigger hyperalgesia, which may be attributed to increased extracellular signal‐regulated kinase (ERK) phosphorylation and participation of c‐JUN.…”

Section: Discussionmentioning

confidence: 99%

Morphine exposure during early life alters thermal and mechanical thresholds in rats

Nunes

Medeiros

Freitas

et al. 2016

Intl J of Devlp Neuroscience

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“…The anti-hyperalgesic effect of these antagonists was largely believed to occur through central NMDARs [1; 46; 49]. Peripheral NMDARs, however, might also have been involved and could constitute better therapeutic targets because of the fewer side effects of NMDAR antagonists that do not cross the blood-brain-barrier [57].…”

Section: Introductionmentioning

confidence: 99%

GluN2B N-methyl-D-aspartate receptor and excitatory amino acid transporter 3 are upregulated in primary sensory neurons after 7 days of morphine administration in rats

Gong

Bhargava

Jasmin

2016

Pain

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The contribution of the peripheral nervous system to opiate-induced hyperalgesia (OIH) is not well understood. Here, we determined the changes in excitability of primary sensory neurons after sustained morphine administration for 7 days. Changes in expression of glutamate receptors and glutamate transporters after morphine administration were ascertained in dorsal root ganglions (DRGs). Patch clamp recordings from intact DRGs (ex-vivo preparation) of morphine-treated rats showed increased excitability of small diameter (≤ 30 μm) neurons with respect to rheobase and membrane threshold, whereas the excitability of large diameter (> 30 μm) neurons remained unchanged. Small diameter neurons also displayed increased responses to glutamate, which were mediated mainly by GluN2B containing NMDA receptors (NMDARs), and to a lesser degree by the neuronal excitatory amino acid transporter 3 /excitatory amino acid carrier 1 (EAAT3/EAAC1). Co-administration in vivo of the GluN2B selective antagonist Ro 25-6981 with morphine for 7 days prevented the appearance of OIH and increased morphine-induced analgesia. Administration of morphine for 7 days led to an increased expression of GluN2B and EAAT3/EAAC1, but not of the AMPA, kainate or Group I metabotropic glutamate receptors, or of the vesicular glutamate transporter 2 (VGLUT2). These results suggest that peripheral glutamatergic neurotransmission contributes to OIH and that GluN2B subunit of NMDARs in the periphery may be a target for therapy.

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N-methyl-D-aspartate receptors involved in morphine-induced hyperalgesia in sensitized mice

Cited by 18 publications

References 44 publications

Differential tolerance to morphine antinociception in assays of pain-stimulated vs. pain-depressed behavior in rats

Differential tolerance to morphine antinociception in assays of pain-stimulated vs. pain-depressed behavior in rats

Morphine exposure during early life alters thermal and mechanical thresholds in rats

GluN2B N-methyl-D-aspartate receptor and excitatory amino acid transporter 3 are upregulated in primary sensory neurons after 7 days of morphine administration in rats

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