Changes in Response Properties and Receptive Fields of Spinal Dorsal Horn Neurons in Rats after Surgical Incision in Hairy Skin

Kawamata, Mikito; Koshizaki, Masayuki; Shimada, Steven G.; Narimatsu, Eichi; Kozuka, Yuji; Takahashi, Toshiyuki; Namiki, Akiyoshi; Collins, J. G.

doi:10.1097/00000542-200501000-00023

Cited by 31 publications

(22 citation statements)

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“…During incision and suturation an increase in activity was recorded in all three classes of spinal neurons, but spontaneous activity and that evoked by light tactile stimulation, as is used to assess allodynia, for several hours after surgery was only prominent in the WDR neurons (Kawamata et al, 2005). Both primary and secondary tactile allodynia were apparent from 30 min to 3-4 days after surgery, in agreement with our own findings in rat hairy skin after an almost identical incision.…”

Section: Discussionsupporting

confidence: 88%

“…We and others have previously shown that central sensitization appears after incision in rat hairy skin, as evidenced by the actions of systemic local anesthetics on post-incisional pain (Duarte et al, 2005) and by recordings from high threshold and low threshold afferents as well as wide dynamic range (WDR) spinal cord neurons (Kawamata et al, 2005). During incision and suturation an increase in activity was recorded in all three classes of spinal neurons, but spontaneous activity and that evoked by light tactile stimulation, as is used to assess allodynia, for several hours after surgery was only prominent in the WDR neurons (Kawamata et al, 2005).…”

Section: Discussionmentioning

confidence: 94%

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Cutaneous endothelin-A receptors elevate post-incisional pain

Mujenda

Duarte

Reilly

et al. 2007

Pain

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The contribution of endothelin-1 (ET-1), acting via endothelin-A receptors (ET A ), on post-incisional pain was examined in a rat model of incision through the hairy skin of the lumbar dorsum. Postincisional mechanical hyperesthesia was evaluated by cutaneous trunci muscle reflexes (CTMR) of subcutaneous muscles responding to stimulation with von Frey filaments near the wound (primary responses) and at a distance, especially on the contralateral dorsum (secondary responses, involving spinal circuits). The role of ET A was determined by pre-incisional, subcutaneous injection of the selective receptor antagonist BQ-123 at the incision site, 15 min or 24 hr before surgery. Control incisions showed both primary tactile allodynia and hyperalgesia, and a weaker secondary hyperesthesia, peaking 3-4 h after surgery and lasting at least 24h. Primary allodynia, but not hyperalgesia, was dose-dependently suppressed by 15 min pre-incisional BQ-123. In contrast, both secondary allodynia and hyperalgesia were inhibited by local BQ-123. The suppression of primary allodynia by local antagonist disappeared in 24 h, but that of secondary hyperesthesia remained strong for at least 24 h. Systemically delivered BQ-123 was without effect on any post-incisional hyperesthesia, and if the antagonist was locally injected 24 h before surgery there was no difference on hyperesthesia compared to vehicle injected at that time. We conclude that ET-1, released from skin by incision, activates nociceptors to cause primary allodynia and to sensitize spinal circuits through central sensitization. Blockade of ET A in the immediate peri-operative period prevents the later development of central sensitization.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 94%

Cutaneous endothelin-A receptors elevate post-incisional pain

Mujenda

Duarte

Reilly

et al. 2007

Pain

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“…Plantar paw incision causes a rapid, transient release of glutamate and aspartate in the spinal cord for the first hour after incision [48], and intrathecal delivery of antagonists of AMPA/kainate receptors [26,31] and of mGluR5 receptors [50], but antagonists of NMDA receptors [47], around the time of incision can reduce the pain elevated by paw incision. These findings suggest that the activation of AMPA/kainate and certain metabotropic glutamate receptors in the spinal cord is important for the induction of pain after skin incision [23,44]. …”

Section: Discussionmentioning

confidence: 99%

“…The initial discharge of local nerves caused by the incision [46] and the later, delayed activation of impulses from peripheral nerve that may be conducted by injured or uninjured fibers [4,5,17,30] probably contribute to the establishment of longer-lasting hyperalgesia [28], and there is little doubt that changes in the central nervous system (CNS), at least at the spinal cord (and probably also in the brain), are essential for the maintained chronic pain [10,23,24]. The differential ability of different drugs, applied at the incision site or delivered systemically, to prevent or reverse postoperative pain supports the concept of at least 2 stages of postoperative pain, an induction stage and a maintenance stage, which involve different mechanisms and occur at different locations [2,12,27].…”

Section: Introductionmentioning

confidence: 99%

Enduring prevention and transient reduction of postoperative pain by intrathecal resolvin D1

Huang

Wang

Serhan

et al. 2011

Pain

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Postoperative pain slows surgical recovery, impacting the return of normal function for weeks, months, or longer. Here we report the antihyperalgesic actions of a new compound, resolvin D1 (RvD1), known to reduce inflammation and to suppress pain after peripheral nerve injury, on the acute pain occurring after paw incision and the prolonged pain after skin-muscle retraction. Injection of RvD1 (20–40 ng) into the L5–L6 intrathecal space 30 minutes before surgery reduces the postincisional primary mechanical hypersensitivity, lowering the peak change by approximately 70% (with 40 ng) and reducing the area under the curve (AUC) for the entire 10-day postincisional course by approximately 60%. Intrathecal injection of RvD1 on postoperative day (POD) 1 reduces the hyperalgesia to the same level as that from preoperative injection within a few hours, an effect that persists for the remaining PODs. Tactile allodynia and hyperalgesia following the skin/muscle incision retraction procedure, measured at the maximum values 12 to 14 days, is totally prevented by intrathecal RvD1 (40 ng) given at POD 2. However, delaying the injection until POD 9 or POD 17 results in RvD1 causing only transient and incomplete reversal of hyperalgesia, lasting for <1 day. These findings demonstrate the potent, effective reduction of postoperative pain by intrathecal RvD1 given before or shortly after surgery. The much more limited effect of this compound on retraction-induced pain, when given 1 to 2 weeks later, suggests that the receptors or pathways for resolvins are more important in the early than the later stages of postoperative pain.

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“…19 32 and increases the sensitivity of WDR neurons to both noxious and non-noxious inputs. 31 These are the first and fundamental steps of central sensitisation. The overall effect is an increased number of action potentials generated in nociceptive pathways ascending to neuromatrix regions.…”

Section: A Peripheral Nociceptorsmentioning

confidence: 99%

Chronic Pain: We Should Not Underestimate the Contribution of Neural Plasticity

Lewis

Rice

2014

Crit Rev Phys Rehabil Med

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Disability associated with chronic pain is a prevalent worldwide problem. Much of our understanding of how and why chronic pain develops has been provided through developments in neural imaging and assessment techniques. Such investigations have highlighted the substantial amount of neural plasticity, or neural reorganisation, that is possible within the nociceptive system. While this plasticity is often physiologically beneficial and usually reverses over time, persistent plasticity can occur following long term activation or damage to the nociceptive system. These adaptations are associated with the development and maintenance of chronic pain conditions. This review provides an outline of the nociceptive system and describes the evidence for plasticity of the system at peripheral, spinal, and supraspinal levels. A number of clinical symptoms associated with chronic pain are described along with the possible neural mechanisms that may contribute to the presentation. Finally, chronic pain management approaches that promote reorganisation of the nociceptive system are discussed. These include sensory training, noninvasive brain stimulation, and mechanisms-based treatment.

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Changes in Response Properties and Receptive Fields of Spinal Dorsal Horn Neurons in Rats after Surgical Incision in Hairy Skin

Cited by 31 publications

References 0 publications

Cutaneous endothelin-A receptors elevate post-incisional pain

Cutaneous endothelin-A receptors elevate post-incisional pain

Enduring prevention and transient reduction of postoperative pain by intrathecal resolvin D1

Chronic Pain: We Should Not Underestimate the Contribution of Neural Plasticity

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