MK-801 reduces non-noxious stimulus-evoked Fos-like immunoreactivity in the spinal cord of rats with chronic constriction nerve injury

Kosai, Kazuko; Tateyama, Shingo; Ikeda, Tetsuya; Uno, Takeshi; Nishimori, Toshikazu; Takasaki, Mayumi

doi:10.1016/s0006-8993(01)02715-9

Cited by 13 publications

(7 citation statements)

References 25 publications

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“… 25 – 27 Although A-fiber–stimulated c-Fos expression was increased in all groups, which was most likely due to the activation Aβ- and Aδ-fiber nociceptors, there was no significant difference in expression between the experimental and untreated groups. This finding contrasts from reports in models of traumatic nerve injury, 25 , 62 , 63 and a model of vincristine-induced neuropathy, 64 and may reflect the minor nature of the injury.…”

Section: Discussioncontrasting

confidence: 99%

Neuritis and vinblastine-induced axonal transport disruption lead to signs of altered dorsal horn excitability

Satkeviciute

Dilley

2018

Mol Pain

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BackgroundMany patients with neuropathic pain present without signs of nerve injury on routine clinical examination. Some of these patients may have inflamed peripheral nerves (neuritis). In this study, we have examined whether neuritis causes changes within the dorsal horn that may contribute to a central pain mechanism. Comparisons have been made to a model of axonal transport disruption induced using vinblastine, since neuritis disrupts such processes.ResultsAt the peak of cutaneous hypersensitivities, recordings from wide dynamic range neurons revealed increases in wind-up following neuritis but not vinblastine treatment. Ongoing activity from these neurons was unchanged. Vinblastine treatment caused a reduction in the responses of wide dynamic range neurons to noxious mechanical stimulation of the receptive field. The response of neurons to innocuous mechanical stimulation was also reduced in wide dynamic range neurons that were at a depth ≥550 µm following vinblastine treatment. An examination of the superficial dorsal horn revealed an increase in c-Fos–positive neurons in both groups following electrical stimulation of the sciatic nerve. The area of dorsal horn expressing substance P was also decreased following vinblastine treatment.ConclusionThese findings indicate that a minor nerve insult, such as neuritis, can lead to changes within the dorsal horn that are consistent with a central neuropathic pain mechanism.

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Section: Discussioncontrasting

confidence: 99%

Neuritis and vinblastine-induced axonal transport disruption lead to signs of altered dorsal horn excitability

Satkeviciute

Dilley

2018

Mol Pain

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“…However, diabetes appears to induce specific effects in spinal cord neurons in what concerns the responses to innocuous stimulation. In several traumatic neuropathic models, innocuous stimuli induce c-fos expression [15,20,[23][24][25], whereas in our diabetic rats the innocuous mechanical stimulus failed to increase c-fos expression in relation to baseline levels, in spite of the long duration of stimulus delivery. Since mechanical allodynia is a feature of diabetic neuropathy [7,8,32], it is likely that the high baseline Fos levels in diabetic animals uncovered any innocuous-evoked increases in c-fos expression induced by innocuous mechanical stimulation.…”

Section: Discussioncontrasting

confidence: 64%

C‐fos expression at the spinal dorsal horn of streptozotocin‐induced diabetic rats

Morgado

Tavares

2007

Diabetes Metabolism Res

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“…The value of the analysis of Fos expression to monitor the nociceptive activity of large neuronal populations is solid (Coggeshall, 2005) and is reinforced by the present findings. Fos expression was previously demonstrated at the spinal cord in several chronic pain models in the absence of additional stimulation, which also occurred in STZ rats (Williams et al, 1991;Kajander et al, 1996;Catheline et al, 1999;Tokunaga et al, 1999;Bester et al, 2000;Dai et al, 2001;Kosai et al, 2001;Tsai et al, 2002;Coggeshall, 2005;Jergova and Cizkova, 2005;Morgado and Tavares, 2007). In the brain of STZ rats, Fos expression was shown to increase in some regions (Zheng et al, 2002;Revsin et al, 2005) and decrease in others (Zheng et al, 2002;Jang et al, 2003;Gouty et al, 2003), showing that it cannot be a direct result of STZ or indicate putative physiological disturbances of diabetic animals.…”

Section: Discussionmentioning

confidence: 82%

Neuronal hyperactivity at the spinal cord and periaqueductal grey during painful diabetic neuropathy: Effects of gabapentin

Morgado

Pereira-Terra

Tavares

2010

European Journal of Pain

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Painful diabetic neuropathy may be due to impairments in descending modulation of nociceptive transmission at the spinal cord. In the present study, streptozotocin diabetic rats (STZ rats) with neuropathic symptoms (mechanical hypersensitivity) were used to perform a time-course evaluation of neuronal activity at the spinal dorsal horn and at the periaqueductal grey matter (PAG), a major brainstem area of pain modulation. The expression of Fos protein, a marker of nociceptive activation, progressively increased at the spinal dorsal horn at 4 and 10 weeks. At the PAG, increases in Fos expression were detected until the 4th week, with a reversal to baseline values at 10 weeks in all areas except the ventrolateral PAG. Co-localisation of Fos with NeuN ascertained the neuronal nature of Fos-expressing cells at the spinal cord and PAG. Four weeks after diabetes induction, the effects of gabapentin (i.p. injection of 50mg/kg, daily during 3 days) were assessed. Gabapentin decreased Fos expression at the spinal cord and PAG and reversed mechanical hypersensitivity. The present study shows that diabetic neuropathy is accompanied by a progressive increase of the spontaneous neuronal activity at the spinal cord. Changes in descending modulation of nociceptive transmission from the PAG are likely to occur during diabetic neuropathy, probably with exacerbation of facilitatory actions. The effects of gabapentin in reversing the behavioural signs of diabetic neuropathy and neuronal hyperactivity in the spinal cord and PAG reinforce the central causes of diabetic neuropathy and point to the central targets of the drug.

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MK-801 reduces non-noxious stimulus-evoked Fos-like immunoreactivity in the spinal cord of rats with chronic constriction nerve injury

Cited by 13 publications

References 25 publications

Neuritis and vinblastine-induced axonal transport disruption lead to signs of altered dorsal horn excitability

Neuritis and vinblastine-induced axonal transport disruption lead to signs of altered dorsal horn excitability

C‐fos expression at the spinal dorsal horn of streptozotocin‐induced diabetic rats

Neuronal hyperactivity at the spinal cord and periaqueductal grey during painful diabetic neuropathy: Effects of gabapentin

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