Time Course of Inflammation in Dorsal Root Ganglia Correlates with Differential Reversibility of Mechanical Allodynia

Noh, Myung-chul; Mikler, Benjamin; Joy, Twinkle; Smith, Peter A.

doi:10.1016/j.neuroscience.2019.12.040

Cited by 19 publications

(39 citation statements)

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“…Finally, the variety of peripheral nerve injury models that have been used provoke different changes in the physiology and behavioral manifestations of pain and nociception (Kim et al, 1997;Lee et al, 1998;Decosterd and Woolf, 2000;Chen et al, 2009b;Stemkowski and Smith, 2013;Noh et al, 2020). This complicates the evaluation, comparison, integration and summation of data from different research groups.…”

Section: Lost In Translationmentioning

confidence: 99%

“…Because a fraction of both sensory and motor axons survive after SNL, SNT, CCI and SNI, animals can be assessed for mechanical and/or thermal hyperalgesia. The main difference between CCI and SNI is that the behavioral responses to CCI subside within a month or so whereas those produced by SNI persist for much longer periods of time (Decosterd and Woolf, 2000;Noh et al, 2020). SNL, SNT, and SNI are thus emerging as preferred animal protocols by which to model human neuropathic pain.…”

Section: Animal Models Of Neuropathic Painmentioning

confidence: 99%

“…This time-dependent replacement of one channel type by another may relate to the partial recovery of mechanical hypersensitivity seen in some nerve injury models such as CCI but not after SNI (Decosterd and Woolf, 2000;Noh et al, 2020).…”

Section: A-channelsmentioning

confidence: 99%

“…It is widely accepted that a transient injury-induced inflammatory event is the primary trigger to the onset of neuropathic pain ( Watkins and Maier, 2002 ; Scholz and Woolf, 2007 ; Kawasaki et al, 2008a , b ; Leung and Cahill, 2010 ; Gaudet et al, 2011 ; Stemkowski and Smith, 2012b ; von Hehn et al, 2012 ; Noh et al, 2020 ). The crucial interplay between the nervous and immune systems ( Ren and Torres, 2009 ) has led some authors to describe neuropathic pain as a neuroimmune disorder ( Scholz and Woolf, 2007 ; Grace et al, 2014 ).…”

Section: Physiological and Pathophysiological Regulation Of K mentioning

confidence: 99%

“…It is recognized, for example, that the processes initiating neuropathic pain (within 1–2 weeks of peripheral nerve injury) differ from those that maintain it over periods of months or years ( Ji et al, 2006 , 2019 ; Zhuang et al, 2006 ). Although the latter phenomena are more relevant to the clinical presentation of neuropathic pain, much of the work done in the laboratory has been associated with investigation of mechanisms underlying pain onset ( Gold and Gebhart, 2010 ; Clark, 2016 ; Noh et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

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K+ Channels in Primary Afferents and Their Role in Nerve Injury-Induced Pain

Smith

2020

Front. Cell. Neurosci.

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Sensory abnormalities generated by nerve injury, peripheral neuropathy or disease are often expressed as neuropathic pain. This type of pain is frequently resistant to therapeutic intervention and may be intractable. Numerous studies have revealed the importance of enduring increases in primary afferent excitability and persistent spontaneous activity in the onset and maintenance of peripherally induced neuropathic pain. Some of this activity results from modulation, increased activity and /or expression of voltage-gated Na + channels and hyperpolarization-activated cyclic nucleotide-gated (HCN) channels. K + channels expressed in dorsal root ganglia (DRG) include delayed rectifiers (K v 1.1, 1.2), A-channels (K v 1.4, 3.3, 3.4, 4.1, 4.2, and 4.3), KCNQ or M-channels (K v 7.2, 7.3, 7.4, and 7.5), ATP-sensitive channels (K IR 6.2), Ca 2+-activated K + channels (K Ca 1.1, 2.1, 2.2, 2.3, and 3.1), Na +-activated K + channels (K Ca 4.1 and 4.2) and two pore domain leak channels (K 2p ; TWIK related channels). Function of all K + channel types is reduced via a multiplicity of processes leading to altered expression and/or post-translational modification. This also increases excitability of DRG cell bodies and nociceptive free nerve endings, alters axonal conduction and increases neurotransmitter release from primary afferent terminals in the spinal dorsal horn. Correlation of these cellular changes with behavioral studies provides almost indisputable evidence for K + channel dysfunction in the onset and maintenance of neuropathic pain. This idea is underlined by the observation that selective impairment of just one subtype of DRG K + channel can produce signs of pain in vivo. Whilst it is established that various mediators, including cytokines and growth factors bring about injury-induced changes in DRG function and excitability, evidence presently available points to a seminal role for interleukin 1β (IL-1β) in control of K + channel function. Despite the current state of knowledge, attempts to target K + channels for therapeutic pain management have met with limited success. This situation may change with the advent of personalized medicine. Identification of specific sensory abnormalities and genetic profiling of individual patients may predict therapeutic benefit of K + channel activators.

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Section: Lost In Translationmentioning

confidence: 99%

Section: Animal Models Of Neuropathic Painmentioning

confidence: 99%

Section: A-channelsmentioning

confidence: 99%

Section: Physiological and Pathophysiological Regulation Of K mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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K+ Channels in Primary Afferents and Their Role in Nerve Injury-Induced Pain

Smith

2020

Front. Cell. Neurosci.

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Establishment of a Magnetically Controlled Scalable Nerve Injury Model

Yang,

Liu,

Cao

et al. 2024

Advanced Science

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Animal models of peripheral nerve injury (PNI) serve as the fundamental basis for the investigations of nerve injury, regeneration, and neuropathic pain. The injury properties of such models, including the intensity and duration, significantly influence the subsequent pathological changes, pain development, and therapeutic efficacy. However, precise control over the intensity and duration of nerve injury remains challenging within existing animal models, thereby impeding accurate and comparative assessments of relevant cases. Here, a new model that provides quantitative and off‐body controllable injury properties via a magnetically controlled clamp, is presented. The clamp can be implanted onto the rat sciatic nerve and exert varying degrees of compression under the control of an external magnetic field. It is demonstrated that this model can accurately simulate various degrees of pathology of human patients by adjusting the magnetic control and reveal specific pathological changes resulting from intensity heterogeneity that are challenging to detect previously. The controllability and quantifiability of this model may significantly reduce the uncertainty of central response and inter‐experimenter variability, facilitating precise investigations into nerve injury, regeneration, and pain mechanisms.

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Platelet‐rich plasma and cytokines in neuropathic pain: A narrative review and a clinical perspective

Bohren

Timbolschi

Müller

et al. 2021

European Journal of Pain

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Background and Objective Neuropathic pain arises as a direct consequence of a lesion or disease affecting the somatosensory system. A number of preclinical studies have provided evidence for the involvement of cytokines, predominantly secreted by a variety of immune cells and by glial cells from the nervous system, in neuropathic pain conditions. Clinical trials and the use of anti‐cytokine drugs in different neuropathic aetiologies support the relevance of cytokines as treatment targets. However, the use of such drugs, in particularly biotherapies, can provoke notable adverse effects. Moreover, it is challenging to select one given cytokine as a target, among the various neuropathic pain conditions. It could thus be of interest to target other proteins, such as growth factors, in order to act more widely on the neuroinflammation network. Thus, platelet‐rich plasma (PRP), an autologous blood concentrate, is known to contain a natural concentration of growth factors and immune system messengers and is widely used in the clinical setting for tissue regeneration and repair. Database and Data Treatment In the present review, we critically assess the current knowledge on cytokines in neuropathic pain by taking into consideration both human studies and animal models. Results This analysis of the literature highlights the pathophysiological importance of cytokines. We particularly highlight the concept of time‐ and tissue‐dependent cytokine activation during neuropathic pain conditions. Conclusion Thus, direct or indirect cytokines modulation with biotherapies or growth factors appears relevant. In addition, we discuss the therapeutic potential of localized injection of PRP as neuropathic pain treatment by pointing out the possible link between cytokines and the action of PRP. Significance Preclinical and clinical studies highlight the idea of a cytokine imbalance in the development and maintenance of neuropathic pain. Clinical trials with anticytokine drugs are encouraging but are limited by a 'cytokine candidate approach' and adverse effect of biotherapies. PRP, containing various growth factors, is a new therapeutic used in regenerative medicine. Growth factors can be also considered as modulators of cytokine balance. Here, we emphasize a potential therapeutic effect of PRP on cytokine imbalance in neuropathic pain. We also underline the clinical interest of the use of PRP, not only for its therapeutic effect but also for its safety of use.

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Time Course of Inflammation in Dorsal Root Ganglia Correlates with Differential Reversibility of Mechanical Allodynia

Cited by 19 publications

References 79 publications

K+ Channels in Primary Afferents and Their Role in Nerve Injury-Induced Pain

K+ Channels in Primary Afferents and Their Role in Nerve Injury-Induced Pain

Establishment of a Magnetically Controlled Scalable Nerve Injury Model

Platelet‐rich plasma and cytokines in neuropathic pain: A narrative review and a clinical perspective

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