RGD Reference Report - A role of the ubiquitin-proteasome system in neuropathic pain. - Rat Genome Database

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A role of the ubiquitin-proteasome system in neuropathic pain.

Authors: Moss, A  Blackburn-Munro, G  Garry, EM  Blakemore, JA  Dickinson, T  Rosie, R  Mitchell, R  Fleetwood-Walker, SM 
Citation: Moss A, etal., J Neurosci 2002 Feb 15;22(4):1363-72.
RGD ID: 70392
Pubmed: PMID:11850463   (View Abstract at PubMed)
PMCID: PMC6757556   (View Article at PubMed Central)

Neuropathic pain (characterized by hyperalgesia and allodynia to mechanical and thermal stimuli) causes cellular changes in spinal dorsal horn neurons, some of which parallel those in synaptic plasticity associated with learning. Ubiquitin C-terminal hydrolase (UCH) appears to play a key role in long-term facilitation in Aplysia. The cooperation of UCH with the proteolytic enzyme complex known as the proteasome is required for the degradation of a number of signaling molecules within the cell that may remove normal restraints on synaptic plasticity. We have used electrophysiology, in situ hybridization histochemistry, semiquantitative RT-PCR, Western blotting, and in vivo behavioral reflex analysis to investigate the ubiquitin-proteasome system in a model of neuropathic pain. In neuropathic animals, ionophoretic application of selective proteasome inhibitors attenuated dorsal horn neuron firing evoked by normally innocuous brush or cold stimuli and by noxious mustard oil stimuli. In control animals, only mustard oil-evoked responses were inhibited. Intrathecal administration of proteasome inhibitors attenuated hyperalgesia and allodynia in neuropathic rats. Expression of UCH-L1 (a rat homolog of Aplysia neuronal UCH and of the human UCH-L1, also known as PGP 9.5) and its mRNA were selectively increased within the ipsilateral dorsal horn of neuropathic rats, supporting the idea of a role for the ubiquitin-proteasome system in nociceptive processing. Proteasome inhibitors selectively attenuate allodynic and hyperalgesic responses in neuropathic pain, with some reduction in normal nociceptive, but not non-nociceptive responses, and potentially represent a novel therapeutic strategy for neuropathic pain.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Uchl1Ratubiquitin-dependent protein catabolic process  IDA  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Uchl1  (ubiquitin C-terminal hydrolase L1)


Additional Information