Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
January 15, 2002Journal of NeuroscienceOpen Access

ERK MAP Kinase Activation in Superficial Spinal Cord Neurons Induces Prodynorphin and NK-1 Upregulation and Contributes to Persistent Inflammatory Pain Hypersensitivity

View Full Paper
Ask AI
Bookmark
Share

Authors

Ru‐Rong JiRu‐Rong JiJiangnan UniversityKBKatia BefortLaboratoire de Neurosciences Cognitives et AdaptativesGBGary J. BrennerHarvard University

Discussion

Loading...

Member takes

Implication

Key Points

Key points are not available for this paper at this time.

Cite This Study

Ji et al. (2002) studied this question.

synapsesocial.com/papers/6a0ef2cc53f874f2b222fd16https://doi.org/10.1523/jneurosci.22-02-00478.2002
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1In situ hybridization histochemistry and immunocytochemistry reveal an increase in spinal dynorphin biosynthesis in a rat model of peripheral inflammation and hyperalgesia.1988 · 290 citations
  2. 2Transcriptional and posttranslational plasticity and the generation of inflammatory pain1999 · 556 citations
  3. 3Phosphorylation of Transcription Factor CREB in Rat Spinal Cord after Formalin-Induced Hyperalgesia: Relationship to c-fos Induction1997 · 213 citations
  4. 4Morphine, the NMDA receptor antagonist MK801 and the tachykinin NK1 receptor antagonist RP67580 attenuate the development of inflammation-induced progressive tactile hypersensitivity1998 · 31 citations