Spatial and temporal aspects of spinal cord and brainstem activation in the formalin pain model

Porro, Carlo Adolfo; Cavazzuti, Milena

doi:10.1016/0301-0082(93)90044-s

Cited by 169 publications

(68 citation statements)

References 449 publications

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“…Peripheral formalin injection has long been used as a model of inflammation (Dubuisson and Dennis, 1977;Tjolsen et al, 1992;Porro and Cavazzuti, 1993). We had previously also found that robust spinal microglia activation was caused by formalin injection (Fu et al, 1999).…”

Section: Cfa Injection Produces More Severe Peripheral Inflammation mentioning

confidence: 98%

Dissociation of spinal microglia morphological activation and peripheral inflammation in inflammatory pain models

Lin

Zhang

et al. 2007

Journal of Neuroimmunology

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We compared the effects of peripheral Freund's Complete Adjuvant (CFA) and formalin injection on spinal microglia activation. Both qualitative and quantitative analyses showed signs of microglia activation on the ipsilateral side of the lumbar dorsal horn on day 3, day 7 and day 14 after formalin injection. However, significant microglia morphological alteration was not found in the CFA model. At the injection site in the paw, CFA injection induced considerably more inflammation than formalin injection. Although spinal microglia might be activated in inflammatory pain models, morphologically, spinal microglia activation was not closely correlated with peripheral inflammation.

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Section: Cfa Injection Produces More Severe Peripheral Inflammation mentioning

confidence: 98%

Dissociation of spinal microglia morphological activation and peripheral inflammation in inflammatory pain models

Lin

Zhang

et al. 2007

Journal of Neuroimmunology

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“…direct formalin stimulation of peripheral nerve endings, whereas the late one is due to subsequent inflammation, MNAC13 appears to be more specifically effective on the inflammatory component of formalin-induced pain (32 2C). …”

Section: Mnac13 Specifically Binds Trka and Leads To Inhibition Of Ngf-mentioning

confidence: 99%

“…To investigate the analgesic potential of blocking NGFmediated activation of the TrkA receptor, the effects of MNAC13 administration were evaluated in a typical model of inflammation-derived persistent pain (formalin-evoked pain) (32) and in the chronic constriction injury (CCI) model of neuropathic pain (33). In addition, because a functional interaction between NGF and opioid system was reported in experimental models of inflammatory pain (34,35), the possible synergistic effects of the anti-TrkA antibody with opiates, such as morphine and fentanyl, were investigated.…”

mentioning

confidence: 99%

The function neutralizing anti-TrkA antibody MNAC13 reduces inflammatory and neuropathic pain

Ugolini¹,

Marinelli

Covaceuszach

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

114

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Nerve growth factor (NGF) is involved in pain transduction mechanisms and plays a key role in many persistent pain states, notably those associated with inflammation. On this basis, both the NGF ligand and its receptor TrkA (tyrosine kinase A) represent an eligible target for pain therapy. Although the direct involvement of NGF in pain modulation is well established, the effect of a direct functional block of the TrkA receptor is still unknown. In this study, we have demonstrated that MNAC13, the only anti-TrkA monoclonal antibody for which function neutralizing properties have been clearly shown both in vitro and in vivo, induces analgesia in both inflammatory and neuropathic pain models, with a surprisingly long-lasting effect in the latter. The formalin-evoked pain licking responses are significantly reduced by the MNAC13 antibody in CD1 mice. Remarkably, treatment with the anti-TrkA antibody also produces a significant antiallodynic effect on neuropathic pain: repeated i.p. injections of MNAC13 induce significant functional recovery in mice subjected to sciatic nerve ligation, with effects persisting after administration. Furthermore, a clear synergistic effect is observed when MNAC13 is administered in combination with opioids, at doses that are not efficacious per se. This study represents a direct demonstration that neutralizing antibodies directed against the TrkA receptor may display potent analgesic effects in inflammatory and chronic pain.analgesia ͉ behavior ͉ mice ͉ nerve growth factor

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“…Further, exogenous treatment with ANX12-26 inhibits nociceptive transmission associated with inflammatory processes in a formalin test, suggesting that ANX1 reduces paw oedema and inflammation (25,(29)(30)(31)(32). Several studies have suggested that inhibition of COX-2 and cytokine production is important for alleviating inflammation, since inflammatory cytokines and COX-2 play important roles in the modulation of inflammation (33)(34)(35).…”

Section: Figmentioning

confidence: 99%

Transduced Tat-Annexin protein suppresses inflammation-associated gene expression in lipopolysaccharide (LPS)-stimulated Raw 264.7 cells

Lee

Kim²,

Back³

et al. 2011

BMB Reports

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Spatial and temporal aspects of spinal cord and brainstem activation in the formalin pain model

Cited by 169 publications

References 449 publications

Dissociation of spinal microglia morphological activation and peripheral inflammation in inflammatory pain models

Dissociation of spinal microglia morphological activation and peripheral inflammation in inflammatory pain models

The function neutralizing anti-TrkA antibody MNAC13 reduces inflammatory and neuropathic pain

Transduced Tat-Annexin protein suppresses inflammation-associated gene expression in lipopolysaccharide (LPS)-stimulated Raw 264.7 cells

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