Nerve injury-induced tactile allodynia is present in the absence of FOS labeling in retrogradely labeled post-synaptic dorsal column neurons

Zhang, En Tan; Ossipov, Michael H.; Zhang, Dong Qin; Lai, Josephine; Porreca, Frank

doi:10.1016/j.pain.2006.10.009

Cited by 21 publications

(16 citation statements)

References 69 publications

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“…The SNT model is a validated and common model to study mechanisms underlying neuropathy-induced pain sensitivity. In line with previous work by Zhang and colleagues, we found that stroking the hindpaw ipsilateral to spinal nerve injury resulted in an increased number of neurons expressing the early neuronal activation marker cFos (Zhang et al, 2007). This increase was observed in the superficial dorsal horn of the lumbar spinal cord.…”

Section: Spinal Gap-43 Expression and Nerve Injurysupporting

confidence: 92%

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Neuropathy-Induced Spinal GAP-43 Expression Is Not a Main Player in the Onset of Mechanical Pain Hypersensitivity

Jaken

Gorp

Joosten

et al. 2011

Journal of Neurotrauma

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Structural plasticity within the spinal nociceptive network may be fundamental to the chronic nature of neuropathic pain. In the present study, the spatiotemporal expression of growth-associated protein-43 (GAP-43), a protein which has been traditionally implicated in nerve fiber growth and sprouting, was investigated in relation to mechanical pain hypersensitivity. An L5 spinal nerve transection model was validated by the presence of mechanical pain hypersensitivity and an increase in the early neuronal activation marker cFos within the superficial spinal dorsal horn upon innocuous hindpaw stimulation. Spinal GAP-43 was found to be upregulated in the superficial L5 dorsal horn from 5 up to 10 days after injury. GAP-43 was co-localized with calcitoningene related peptide (CGRP), but not vesicular glutamate transporter-1 (VGLUT-1), IB4, or protein kinase-c (PKC-c), suggesting the regulation of GAP-43 in peptidergic nociceptive afferents. These GAP-43/CGRP fibers may be indicative of sprouting peptidergic fibers. Fiber sprouting largely depends on growth factors, which are typically associated with neuro-inflammatory processes. The putative role of neuropathy-induced GAP-43 expression in the development of mechanical pain hypersensitivity was investigated using the immune modulator propentofylline. Propentofylline treatment strongly attenuated the development of mechanical pain hypersensitivity and glial responses to nerve injury as measured by microglial and astroglial markers, but did not affect neuropathy-induced levels of spinal GAP-43 or GAP-43 regulation in CGRP fibers. We conclude that nerve injury induces structural plasticity in fibers expressing CGRP, which is regarded as a main player in central sensitization. Our data do not, however, support a major role of these structural changes in the onset of mechanical pain hypersensitivity.

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Section: Spinal Gap-43 Expression and Nerve Injurysupporting

confidence: 92%

“…Five days following SNT, another cohort of animals (n = 6) received non-nociceptive stimulation as previously described (Zhang et al, 2007). The animals were habituated to the experimenter.…”

Section: Non-nociceptive Stimulation Of L5 Snt Animalsmentioning

confidence: 99%

Neuropathy-Induced Spinal GAP-43 Expression Is Not a Main Player in the Onset of Mechanical Pain Hypersensitivity

Jaken

Gorp

Joosten

et al. 2011

Journal of Neurotrauma

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“…Previous studies have demonstrated that normally non-noxious stimulation, such as light touch, produces FOS expression within the spinal dorsal horn of rats with CFA induced inflammation 24 . FOS is an early oncogene that is selectively expressed in response to neuronal activation 24 , and is not normally observed in the spinal dorsal horn in the absence of noxious stimulation in the absence of injury 24, 34, 44 . Spinal FOS expression in response to normally non-noxious stimulation has been used to measure the development of injury-induced spinal sensitization across models of inflammation-, nerve-injury- and cancer-induced pain states 24, 34, 44 .…”

Section: Discussionmentioning

confidence: 99%

“…FOS is an early oncogene that is selectively expressed in response to neuronal activation 24 , and is not normally observed in the spinal dorsal horn in the absence of noxious stimulation in the absence of injury 24, 34, 44 . Spinal FOS expression in response to normally non-noxious stimulation has been used to measure the development of injury-induced spinal sensitization across models of inflammation-, nerve-injury- and cancer-induced pain states 24, 34, 44 . Our observations demonstrate that movement of the MIA treated knee joint selectively induces FOS expression in the spinal dorsal horn of high dose MIA treated rats.…”

Section: Discussionmentioning

confidence: 99%

“…Expression of the early oncogene, FOS, within the spinal dorsal horn in response to normally non-noxious stimulation such as touch 24, 44 or non-noxious palpation 16, 34 has been used as a marker of the development of spinal sensitization. Another key component of central sensitization is descending pain facilitatory pathways from the rostral ventromedial medulla (RVM) 28 .…”

Section: Introductionmentioning

confidence: 99%

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Central Sensitization and Neuropathic Features of Ongoing Pain in a Rat Model of Advanced Osteoarthritis

Havelin

Imbert

Cormier

et al. 2016

The Journal of Pain

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Osteoarthritis (OA) pain is most commonly characterized by movement-triggered joint pain. However, in advanced disease, OA pain becomes persistent, ongoing and resistant to treatment with NSAIDs. The mechanisms underlying ongoing pain in advanced OA are poorly understood. We recently showed that intra-articular (i.a.) injection of monosodium iodoacetate (MIA) into the rat knee joint produces concentration-dependent outcomes. Thus, a low dose of i.a. MIA produces NSAID-sensitive weight asymmetry without evidence of ongoing pain while a high i.a. MIA dose produces weight asymmetry and NSAID-resistant ongoing pain. In the present studies, palpation of the ipsilateral hindlimb of rats treated 14 days previously with high, but not low, doses of i.a. MIA produced FOS expression in the spinal dorsal horn. Inactivation of descending pain facilitatory pathways by microinjection of lidocaine within the rostral ventromedial medulla (RVM) induced conditioned place preference (CPP) selectively in rats treated with the high dose of MIA. CPP to intra-articular lidocaine was blocked by pretreatment with duloxetine (30 mg/kg, i.p. at −30 min). These observations are consistent with the likelihood of a neuropathic component of OA that elicits ongoing, NSAID resistant pain and central sensitization that is mediated, in part, by descending modulatory mechanisms. This model provides a basis for exploration of underlying mechanisms promoting neuropathic components of OA pain and for the identification of mechanisms that may guide drug discovery for treatment of advanced OA pain without the need for joint replacement.

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Single high‐concentration capsaicin application prevents c‐Fos expression in spinothalamic and postsynaptic dorsal column neurons after surgical incision

Uchytilova

Spicarova

Paleček

2015

European Journal of Pain

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Nerve injury-induced tactile allodynia is present in the absence of FOS labeling in retrogradely labeled post-synaptic dorsal column neurons

Cited by 21 publications

References 69 publications

Neuropathy-Induced Spinal GAP-43 Expression Is Not a Main Player in the Onset of Mechanical Pain Hypersensitivity

Neuropathy-Induced Spinal GAP-43 Expression Is Not a Main Player in the Onset of Mechanical Pain Hypersensitivity

Central Sensitization and Neuropathic Features of Ongoing Pain in a Rat Model of Advanced Osteoarthritis

Single high‐concentration capsaicin application prevents c‐Fos expression in spinothalamic and postsynaptic dorsal column neurons after surgical incision

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