Quantitative assessment of tactile allodynia in the rat paw

Chaplan, Sandra R.; Bach, Flemming W.; Pogrel, J. W.; Chung, Jin Mo; Yaksh, Tony L.

doi:10.1016/0165-0270(94)90144-9

Cited by 6,676 publications

(4,730 citation statements)

References 22 publications

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“…All rats were acclimated to the testing environment for at least (the constant 13 refers to the cutoff time). Mechanical sensitivity was assessed with Von Frey hairs, using the updown method [28] and the paw-withdrawal threshold. Each stimulus consisted of 2-3 s application of the Von Frey hair to the plantar surface of the paw, and the inter-stimulus interval was 5 min.…”

Section: Nociception Testsmentioning

confidence: 99%

Toll-like receptor 4-mediated nuclear factor-κB activation in spinal cord contributes to chronic morphine-induced analgesic tolerance and hyperalgesia in rats

et al. 2014

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Nuclear factor kappa B (NF-κB) in the spinal cord is involved in pro-infl ammatory cytokine-mediated pain facilitation. However, the role of NF-κB activation in chronic morphine-induced analgesic tolerance and the underlying mechanisms remain unclear. In the present study, we found that the level of phosphorylated NF-κB p65 (p-p65) was increased in the dorsal horn of the lumbar 4-6 segments after intrathecal administration of morphine for 7 consecutive days, and the p-p65 was co-localized with neurons and astrocytes. The expression of TNF-α and IL-1β was also increased in the same area. In addition, pretreatment with pyrrolidinedithiocarbamate (PDTC) or SN50, inhibitors of NF-κB, prevented the development of morphine analgesic tolerance and alleviated morphine withdrawal-induced allodynia and hyperalgesia. The increase in TNF-α and IL-1β expression induced by chronic morphine exposure was also partially blocked by PDTC pretreatment. In another experiment, rats receiving PDTC or SN50 beginning on day 7 of morphine injection showed partial recovery of the anti-nociceptive effects of morphine and attenuation of the withdrawal-induced abnormal pain. Meanwhile, intrathecal pretreatment with lipopolysaccharide from Rhodobacter sphae roides, an antagonist of toll-like receptor 4 (TLR4), blocked the activation of NF-κB, and prevented the development of morphine tolerance and withdrawalinduced abnormal pain. These data indicated that TLR4-mediated NF-κB activation in the spinal cord is involved in the development and maintenance of morphine analgesic tolerance and withdrawalinduced pain hypersensitivity.

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Section: Nociception Testsmentioning

confidence: 99%

Toll-like receptor 4-mediated nuclear factor-κB activation in spinal cord contributes to chronic morphine-induced analgesic tolerance and hyperalgesia in rats

et al. 2014

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“…Animals were habituated to the testing apparatus for at least 40 min before testing. Each animal was subjected to the stimulation of a series of von Frey filaments (Stoelting, Wood Dale, IL) ranging from 0.008 to 2 g (log force 1.65, 2.36, 2.44, 2.83, 3.22, 3.84, 4.08, 4.17 and 4.31) using the Up-Down paradigm (detailed in [34]). The selected von Frey filament was pressed against the plantar surface of the ipsilateral (side of surgery) hind paw to the point of 30 bending for 3 s. Paw withdrawal response was considered as the positive response.…”

Section: Assessment Of Mechanical Sensitivitymentioning

confidence: 99%

CNS‐infiltrating CD4⁺ T lymphocytes contribute to murine spinal nerve transection‐induced neuropathic pain

2008

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We previously reported leukocytic infiltration into the lumbar spinal cord in a rodent spinal nerve L5 transection (L5Tx) neuropathic pain model. Here, we further investigated the role of infiltrating T lymphocytes in the etiology of persistent pain following L5Tx. T lymphocyte-deficient nude mice showed no evident mechanical hypersensitivity after day 3 of L5Tx compared to wild-type BALB/c mice. Through FACS analysis, we determined that significant leukocytic infiltration (CD45 hi ) into the lumbar spinal cord peaked at day 7 post L5Tx. These infiltrating leukocytes contained predominantly CD4 + but not CD8 + T lymphocytes. B lymphocytes, natural killer cells and macrophages were not detected at day 7 post L5Tx. No differences in the activation of peripheral CD4 + T lymphocytes were detected in either the spleen or lumbar lymph nodes between L5Tx and sham surgery groups. Further, CD4 KO mice displayed significantly decreased mechanical hypersensitivity after day 7 of L5Tx, and adoptive transfer of CD4 + leukocytes reversed this effect. Decreased immunoreactivity of glial fibrillary acidic protein observed in CD4 KO mice post L5Tx indicated possible T lymphocyte-glial interactions. These results strongly support a contributing role of spinal cord-infiltrating CD4 + T lymphocytes versus peripheral CD4 + T lymphocytes in the maintenance of nerve injury-induced neuropathic pain.

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“…75 Animals were placed in a plexiglass box with an elevated mesh floor. After the animal was acclimated for 5 min, calibrated Von Frey hairs with ranges from 0.41 to 8.5g were applied perpendicular to the midplantar area of the ligated and sham-operated hindpaw and depressed slowly until bent.…”

Section: Gene Therapymentioning

confidence: 99%

Amelioration of chronic neuropathic pain after partial nerve injury by adeno-associated viral (AAV) vector-mediated over-expression of BDNF in the rat spinal cord

et al. 2002

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Changing the levels of neurotrophins in the spinal cord micro-environment after nervous system injury has been proposed to recover normal function, such that behavioral response to peripheral stimuli does not lead to chronic pain. We have investigated the effects of recombinant adenoassociated viral (rAAV)-mediated over-expression of brainderived neurotrophic factor (BDNF) in the spinal cord on chronic neuropathic pain after unilateral chronic constriction injury (CCI) of the sciatic nerve. The rAAV-BDNF vector was injected into the dorsal horn at the thirteenth thoracic

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Quantitative assessment of tactile allodynia in the rat paw

Cited by 6,676 publications

References 22 publications

Toll-like receptor 4-mediated nuclear factor-κB activation in spinal cord contributes to chronic morphine-induced analgesic tolerance and hyperalgesia in rats

Toll-like receptor 4-mediated nuclear factor-κB activation in spinal cord contributes to chronic morphine-induced analgesic tolerance and hyperalgesia in rats

CNS‐infiltrating CD4⁺ T lymphocytes contribute to murine spinal nerve transection‐induced neuropathic pain

Amelioration of chronic neuropathic pain after partial nerve injury by adeno-associated viral (AAV) vector-mediated over-expression of BDNF in the rat spinal cord

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Quantitative assessment of tactile allodynia in the rat paw

Cited by 6,676 publications

References 22 publications

Toll-like receptor 4-mediated nuclear factor-κB activation in spinal cord contributes to chronic morphine-induced analgesic tolerance and hyperalgesia in rats

Toll-like receptor 4-mediated nuclear factor-κB activation in spinal cord contributes to chronic morphine-induced analgesic tolerance and hyperalgesia in rats

CNS‐infiltrating CD4+ T lymphocytes contribute to murine spinal nerve transection‐induced neuropathic pain

Amelioration of chronic neuropathic pain after partial nerve injury by adeno-associated viral (AAV) vector-mediated over-expression of BDNF in the rat spinal cord

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CNS‐infiltrating CD4⁺ T lymphocytes contribute to murine spinal nerve transection‐induced neuropathic pain