Antiallodynic Effects of Systemic and Intrathecal Morphine in the Spared Nerve Injury Model of Neuropathic Pain in Rats

Zhao, Cheng; Tall, Jill M.; Meyer, Richard A.; Raja, Srinivasa N.

doi:10.1097/00000542-200404000-00021

Cited by 60 publications

(31 citation statements)

References 43 publications

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“…Zhao et al (35) reported that i.t. morphine administration is likely to be more effective than s.c. injection in the treatment of neuropathic pain.…”

Section: Discussionmentioning

confidence: 99%

Intrathecal herpes simplex virus type 1 amplicon vector-mediated human proenkephalin reduces chronic constriction injury-induced neuropathic pain in rats

et al. 2011

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Abstract. in the present study, we investigated the antinociceptive effect of herpes simplex virus type 1 (HSV-1) amplicon vector-mediated human proenkephalin (hPPe) on chronic constriction injury (cci)-induced neuropathic pain in rats. Male Sprague-dawley rats were intrathecally administered normal saline (nS), pHSVireS-lacZ (SHZ) or recombinant HSV-1 amplicon vector pHSVireS-hPPe-lacZ (SHPZ), respectively. once a week for 5 weeks after the intrathecal (i.t.) administration, the expression levels of hPPe mrna and leu-enkephalin (l-eK) were determined. The paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTl) were measured before cci (baseline) on day 3 and once a week for 5 weeks after i.t. administration. The results showed that the PWMT and PWTl in the SHPZ group were significantly increased compared to the thresholds before i.t. administration. The antinociceptive effect of SHPZ reached its peak 3 weeks after i.t. administration and was maintained for 5 weeks. in the rats administered vehicle or SHZ, there were no significant differences between the PWMT or PWTl and the thresholds before i.t. administration. These results indicate that a single i.t. administration of HSV-1 amplicon vector-mediated hPPe attenuated cci-induced hypersensitivity in rats.

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“…Zhao et al (35) reported that i.t. morphine administration is likely to be more effective than s.c. injection in the treatment of neuropathic pain.…”

Section: Discussionmentioning

confidence: 99%

Intrathecal herpes simplex virus type 1 amplicon vector-mediated human proenkephalin reduces chronic constriction injury-induced neuropathic pain in rats

et al. 2011

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“…*po0.05, **po0.01, ***po0.001 vs sham group. Zhao et al, 2004). Additionally, it has been reported that i.t.…”

Section: Inhibition Of Morphine-or Oxycodone-induced Place Preferencementioning

confidence: 99%

Comparative Pharmacological Profiles of Morphine and Oxycodone under a Neuropathic Pain-Like State in Mice: Evidence for Less Sensitivity to Morphine

Narita

Nakamura

Masahiko

et al. 2007

Neuropsychopharmacol

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The present study was undertaken to investigate pharmacological actions induced by morphine and oxycodone under a neuropathic pain-like state. In the m-opioid receptor (MOR) binding study and G-protein activation, we confirmed that both morphine and oxycodone showed MOR agonistic activities. Mice with sciatic nerve ligation exhibited the marked neuropathic pain-like behavior. Under these conditions, antinociception induced by subcutaneously (s.c.) injected morphine was significantly decreased by sciatic nerve ligation, whereas s.c. injection of oxycodone produced a profound antinociception in sciatic nerve-ligated mice. There were no significant differences in spinal or supraspinal antinociception of morphine and oxycodone between sham operation and nerve ligation. Moreover, either morphine-or oxycodone-induced increase in guanosine-5 0 -o-(3-thio) triphosphate ([ 35 S]GTPgS) binding in the spinal cord, periaqueductal gray matter and thalamus in sciatic nerve-ligated mice was similar to that in sham-operated mice. Antinociception induced by s.c., intrathecal, or intracerebroventricular injection of the morphine metabolite morphine-6-glucuronide (M-6-G) was significantly decreased by sciatic nerve ligation. Furthermore, the increase in the G-protein activation induced by M-6-G was eliminated in sciatic nerve ligation. In addition, either morphine-or oxycodone-induced rewarding effect was dramatically suppressed under a neuropathic pain-like state. The increased [ 35 S]GTPgS binding by morphine or oxycodone was significantly lower in the lower midbrain of mice with sciatic nerve ligation compared with that in control mice. These findings provide further evidence that oxycodone shows a profound antinociceptive effect under a neuropathic pain-like state with less of a rewarding effect. Furthermore, the reduction in G-protein activation induced by M-6-G may, at least in part, contribute to the suppression of the antinociceptive effect produced by morphine under a neuropathic pain-like state.

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“…125 However, in electrophysiological studies, systemic morphine was less effective than morphine administered via direct spinal application in the inhibition of C-fiber, heat, and mechanical stimulation-evoked activity in dorsal horn neurons 128 and intrathecal administration of morphine has been shown to be effective in reversing mechanical allodynia. 129 Intrathecal ␣2 agonists reverse SNL-induced mechanical allodynia. 130 This is substantiated by recent work indicating that intrathecal ␣2 agonists exacerbate thermal hyperalgesia after SNL.…”

Section: Sciatic Nerve Ligationmentioning

confidence: 99%

“…19 The mechanical allodynia is more prominent in hairy skin. 129 Strain differences influence the extent of the pain behavior (Lewis rats are least affected), but all strains exhibit mechanical sensitivity. 134 Late sprouting of sympathetic fibers into the DRG is documented at 8 weeks post-injury, resulting in basket structures around the neuronal stomata.…”

Section: Sciatic Nerve Ligationmentioning

confidence: 99%

“…136 Systemic morphine dose dependently reduces mechanical allodynia and hyperalgesia, as well as cold allodynia. 129,134,137 Spinal morphine is also effective in blocking mechanical allodynia. 129,134 However, Decosterd et al 138 found that systemic morphine, amitriptyline, and carbamazepine produced only modest reversal of mechanical and cold allodynia.…”

Section: Sciatic Nerve Ligationmentioning

confidence: 99%

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Behavioral Models of Pain States Evoked by Physical Injury to the Peripheral Nerve

Sorkin

Yaksh

2009

Neurotherapeutics

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Summary:Physical injury or compression of the root, dorsal root ganglion, or peripheral sensory axon leads to welldefined changes in biology and function. Behaviorally, humans report ongoing painful dysesthesias and aberrations in function, such that an otherwise innocuous stimulus will yield a pain report. These behavioral reports are believed to reflect the underlying changes in nerve function after injury, wherein increased spontaneous activity arises from the neuroma and dorsal root ganglion and spinal changes increase the response of spinal projection neurons. These pain states are distinct from those associated with tissue injury and pose particular problems in management. To provide for developing an understanding of the underlying mechanisms of these pain states and to promote development of therapeutic agents, preclinical models involving section, compression, and constriction of the peripheral nerve or compression of the dorsal root ganglion have been developed. These models give rise to behaviors, which parallel those observed in the human after nerve injury. The present review considers these models and their application.

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Antiallodynic Effects of Systemic and Intrathecal Morphine in the Spared Nerve Injury Model of Neuropathic Pain in Rats

Cited by 60 publications

References 43 publications

Intrathecal herpes simplex virus type 1 amplicon vector-mediated human proenkephalin reduces chronic constriction injury-induced neuropathic pain in rats

Intrathecal herpes simplex virus type 1 amplicon vector-mediated human proenkephalin reduces chronic constriction injury-induced neuropathic pain in rats

Comparative Pharmacological Profiles of Morphine and Oxycodone under a Neuropathic Pain-Like State in Mice: Evidence for Less Sensitivity to Morphine

Behavioral Models of Pain States Evoked by Physical Injury to the Peripheral Nerve

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