The role of the dorsal columns in neuropathic behavior: evidence for plasticity and non-specificity

Saadé, Nayef E.; Baliki, Marwan N.; El-Khoury, C; Hawwa, N; Atweh, Samir; Apkarian, A. Vania; Jabbur, Suhayl J.

doi:10.1016/s0306-4522(02)00417-7

Cited by 38 publications

(9 citation statements)

References 47 publications

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“…However, it seems unlikely that rostral ventromedial medulla facilitation is responsible for prolonged allodynia measured here, since section of the dorso-lateral funiculus, anterolateral columns, and spinal hemi-section (Saade et al, 2006), as well as bilateral section of the dorsal columns (Saade et al, 2002), results in significant but temporary (1–3 week) decreases of allodynia.…”

Section: Discussionmentioning

confidence: 77%

Caudal Granular Insular Cortex Is Sufficient and Necessary for the Long-Term Maintenance of Allodynic Behavior in the Rat Attributable to Mononeuropathy

Benison¹,

Chumachenko²,

Harrison³

et al. 2011

J. Neurosci.

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Mechanical allodynia, the perception of innocuous tactile stimulation as painful, is a severe symptom of chronic pain often produced by damage to peripheral nerves. Allodynia affects millions of people and remains highly resistant to classic analgesics and therapies. Neural mechanisms for the development and maintenance of allodynia have been investigated in the spinal cord, brainstem, thalamus, and forebrain, but manipulations of these regions rarely produce lasting effects. We found that long-term alleviation of allodynic manifestations is produced by discreetly lesioning a newly discovered somatosensory representation in caudal granular insular cortex (CGIC) in the rat, either before or after a chronic constriction injury of the sciatic nerve. However, CGIC lesions alone have no effect on normal mechanical stimulus thresholds. In addition, using electrophysiological techniques, we reveal a corticospinal loop that could be the anatomical source of CGIC’s influence on allodynia.

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Section: Discussionmentioning

confidence: 77%

Caudal Granular Insular Cortex Is Sufficient and Necessary for the Long-Term Maintenance of Allodynic Behavior in the Rat Attributable to Mononeuropathy

Benison¹,

Chumachenko²,

Harrison³

et al. 2011

J. Neurosci.

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“…The DRG develops hyperexcitability after multiple ion channels in injured afferent neurons were altered to produce a bigger generator potential of transduction channel to sensitize to a given natural stimulus or decrease threshold of sodium channels responsible for spike initiation, resulting in their transductions to DRG of those signals. This is one of the possible mechanisms of neuropathic pain ( Saadé et al ., 2002 ; Campbell and Meyer, 2006 ).…”

Section: Discussionmentioning

confidence: 99%

Enhanced Expression of TREK-1 Is Related with Chronic Constriction Injury of Neuropathic Pain Mouse Model in Dorsal Root Ganglion

Han

Lee

Kim

et al. 2016

Biomol Ther (Seoul)

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Neuropathic pain is a complex state showing increased pain response with dysfunctional inhibitory neurotransmission. The TREK family, one of the two pore domain K+ (K2P) channel subgroups were focused among various mechanisms of neuropathic pain. These channels influence neuronal excitability and are thought to be related in mechano/thermosensation. However, only a little is known about the expression and role of TREK-1 and TREK-2, in neuropathic pain. It is performed to know whether TREK-1 and/or 2 are positively related in dorsal root ganglion (DRG) of a mouse neuropathic pain model, the chronic constriction injury (CCI) model. Following this purpose, Reverse Transcription Polymerase Chain Reaction (RT-PCR) and western blot analyses were performed using mouse DRG of CCI model and compared to the sham surgery group. Immunofluorescence staining of isolectin-B4 (IB4) and TREK were performed. Electrophysiological recordings of single channel currents were analyzed to obtain the information about the channel. Interactions with known TREK activators were tested to confirm the expression. While both TREK-1 and TREK-2 mRNA were significantly overexpressed in DRG of CCI mice, only TREK-1 showed significant increase (∼9 fold) in western blot analysis. The TREK-1-like channel recorded in DRG neurons of the CCI mouse showed similar current-voltage relationship and conductance to TREK-1. It was easily activated by low pH solution (pH 6.3), negative pressure, and riluzole. Immunofluorescence images showed the expression of TREK-1 was stronger compared to TREK-2 on IB4 positive neurons. These results suggest that modulation of the TREK-1 channel may have beneficial analgesic effects in neuropathic pain patients.

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“…Increasing evidence suggests that SCS analgesia is intricately linked with spinal segmental mechanisms (Meyerson and Linderoth, 2000;Guan et al, 2010b). Although the dorsal column system may also be involved in the processing of altered somatosensory information during neuropathic conditions (Sun et al, 2001;Saade et al, 2002), lesion studies have shown that a large portion of the analgesic effect produced by SCS is mediated through the dorsal column. Therefore, the primary goal of SCS is to activate the dorsal column, which contains axons that originate in the large-diameter afferent sensory neurons (e.g., Aβ-fibres).…”

Section: Discussionmentioning

confidence: 99%

Comparison of intensity‐dependent inhibition of spinal wide‐dynamic range neurons by dorsal column and peripheral nerve stimulation in a rat model of neuropathic pain

Yang

Cheong

et al. 2014

European Journal of Pain

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Background Spinal cord stimulation (SCS) and peripheral nerve stimulation (PNS) are thought to reduce pain by activating a sufficient number of large myelinated (Aβ) fibres, which in turn initiate spinal segmental mechanisms of analgesia. However, the volume of neuronal activity and how this activity is associated with different treatment targets is unclear under neuropathic pain conditions. Methods We sought to delineate the intensity-dependent mechanisms of SCS and PNS analgesia by in vivo extracellular recordings from spinal wide-dynamic range neurons in nerve-injured rats. To mimic therapeutic SCS and PNS, we used bipolar needle electrodes and platinum hook electrodes to stimulate the dorsal column and the tibial nerve, respectively. Compound action potentials were recorded to calibrate the amplitude of conditioning stimulation required to activate A-fibres and thus titrate the volume of activation. Results Dorsal column stimulation (50 Hz, five intensities) inhibited the windup (a short form of neuronal sensitization) and the C-component response of wide-dynamic range neurons to graded intracutaneous electrical stimuli in an intensity-dependent manner. Tibial nerve stimulation (50 Hz, three intensities) also suppressed the windup in an intensity-dependent fashion but did not affect the acute C-component response. Conclusions SCS and PNS may offer similar inhibition of short-term neuronal sensitization. However, only SCS attenuates spinal transmission of acute noxious inputs under neuropathic pain conditions. Our findings begin to differentiate peripheral from spinal-targeted neuromodulation therapies and may help to select the best stimulation target and optimum therapeutic intensity for pain treatment.

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The role of the dorsal columns in neuropathic behavior: evidence for plasticity and non-specificity

Cited by 38 publications

References 47 publications

Caudal Granular Insular Cortex Is Sufficient and Necessary for the Long-Term Maintenance of Allodynic Behavior in the Rat Attributable to Mononeuropathy

Caudal Granular Insular Cortex Is Sufficient and Necessary for the Long-Term Maintenance of Allodynic Behavior in the Rat Attributable to Mononeuropathy

Enhanced Expression of TREK-1 Is Related with Chronic Constriction Injury of Neuropathic Pain Mouse Model in Dorsal Root Ganglion

Comparison of intensity‐dependent inhibition of spinal wide‐dynamic range neurons by dorsal column and peripheral nerve stimulation in a rat model of neuropathic pain

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