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The pharmacology of Adrenomedullin 2/Intermedin
TLDR
In tissues and in animals it is frequently antagonised by CGRP and AM antagonists; however, situations exist in which an AM2 response is maintained even in the presence of supramaximal concentrations of these antagonists.
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Effect of Mas‐related gene (Mrg) receptors on hyperalgesia in rats with CFA‐induced inflammation via direct and indirect mechanisms
TLDR
The effects of MrgC receptor activation on inflammatory hyperalgesia and its mechanisms are investigated in trigeminal and dorsal root ganglia of DRG.
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The involvement of spinal bovine adrenal medulla 22‐like peptide, the proenkephalin derivative, in modulation of nociceptive processing
TLDR
Results demonstrate for the first time that BAM22‐like peptide is mainly located in the superficial laminae of the spinal cord and mostly originates from nociceptive DRG neurons.
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Sensory neuron-specific receptor agonist BAM8-22 inhibits the development and expression of tolerance to morphine in rats
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Topical and systemic administrations of ketanserin attenuate hypersensitivity and expression of CGRP in rats with spinal nerve ligation.
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p75 Neurotrophin Receptor Protects Primary Cultures of Human Neurons against Extracellular Amyloid β Peptide Cytotoxicity
TLDR
It is found that A β1-40 and Aβ1-42, but not the reverse control peptide, Aβ40-1, rapidly increase the levels of p75NTR in a specific and dose-dependent manner, consistent with a neuroprotective role for p75 NTR against extracellular Aβ toxicity in human neurons.
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Upregulation of adrenomedullin in the spinal cord and dorsal root ganglia in the early phase of CFA-induced inflammation in rats
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A Role for Protein Kinase C-Dependent Upregulation of Adrenomedullin in the Development of Morphine Tolerance in Male Rats
TLDR
Results reveal that a sustained opiate treatment induces an upregulation of AM through the activation of μ-opioid receptors and the PKC signaling pathway, which contributes to the development of tolerance to the antinociceptive effects of opiates at least partially via the up regulation of CGRP.
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Blockade of adrenomedullin receptors reverses morphine tolerance and its neurochemical mechanisms
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[MrgC receptor activation reverses chronic morphine-evoked alterations of glutamate transporters and nNOS in rats].
TLDR
The results suggest that the modulation of pro-nociceptive mediators in the spinal cord and DRG underlies the inhibition of morphine tolerance by MrgC receptor activation.
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