The endogenous fatty acid amide, palmitoylethanolamide, has anti-allodynic and anti-hyperalgesic effects in a murine model of neuropathic pain: involvement of CB1, TRPV1 and PPARγ receptors and neurotrophic factors

@article{Costa2008TheEF,
  title={The endogenous fatty acid amide, palmitoylethanolamide, has anti-allodynic and anti-hyperalgesic effects in a murine model of neuropathic pain: involvement of CB1, TRPV1 and PPAR$\gamma$ receptors and neurotrophic factors},
  author={Barbara Costa and Francesca Comelli and Isabella Bettoni and Mariapia Colleoni and Gabriella Giagnoni},
  journal={PAIN},
  year={2008},
  volume={139},
  pages={541-550}
}
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Increasing CNS FAA levels alone does not lead to robust amelioration of below-level neuropathic SCI pain, and utilizing FAAH inhibition in conjunction with other analgesic mechanisms could be an effective analgesic therapy.
The role of transient receptor potential vanilloid receptor 1 and peroxisome proliferator-activated receptors-&agr; in mediating the antinociceptive effects of palmitoylethanolamine in rats
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Molecular evidence for the involvement of PPAR-δ and PPAR-γ in anti-inflammatory and neuroprotective activities of palmitoylethanolamide after spinal cord trauma
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N-palmitoylethanolamide in the anterior cingulate cortex attenuates inflammatory pain behaviour indirectly via a CB1 receptor-mediated mechanism
TLDR
Data indicate that PEA in the ACC can reduce inflammatory pain-related behaviour, possibly via AEA-induced activation of CB1 receptors and associated modulation of neuronal activity in the basolateral amygdala.
Non-neuronal cell modulation relieves neuropathic pain: efficacy of the endogenous lipid palmitoylethanolamide.
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TLDR
The rationale of using natural remedies in conjunction with classical pharmacological agents to treat chronic NP is supported, as Noxiall was efficacious also in reducing CCI-induced thermal hyperalgesia.
Full Inhibition of Spinal FAAH Leads to TRPV1-Mediated Analgesic Effects in Neuropathic Rats and Possible Lipoxygenase-Mediated Remodeling of Anandamide Metabolism
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It is suggested that intrathecally injected URB597 at full analgesic efficacy unmasks a secondary route of AEA metabolism via 15-LOX with possible formation of 15-hydroxy-AEA, which, together with OEA and PEA, may contribute at producing TRPV1-mediated analgesia in CCI rats.
The Interaction Between Intrathecal Administration of Low Doses of Palmitoylethanolamide and AM251 in Formalin-Induced Pain Related Behavior and Spinal Cord IL1-β Expression in Rats
TLDR
The findings suggest the possible involvement of receptors other than CB1 receptors in spinal pain pathways, such as GPR55, in pain modulating activity of cannabinoids.
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Evidence is provided that PEA activates nNOS, thus initiating the NO/cGMP pathway and inducing peripheral antinociceptive effects, and that exogenous PEA is able to induce NO release.
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