GlyR α3: An Essential Target for Spinal PGE2-Mediated Inflammatory Pain Sensitization

By R. Harvey, Ulrike B. Depner, H. Wässle, Seifollah Ahmadi, Cornelia Heindl, H. Reinold, T. Smart, K. Harvey, B. Schütz, O. Abo-Salem and 7 more. Science, 2004

623 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/b24a30dff4bbb40c6a0f3b9e930edeae63ec7a2c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. R. Ji
2. Clifford J. Woolf
3. Maiken Nedergaard
4. M. Sofroniew
5. Arne May

In Pharmacology

1. R. Ji
2. Clifford J. Woolf
3. T. Berta
4. Maiken Nedergaard
5. Jürgen Sandkühler
6. Alban Latremoliere
7. Linda R. Watkins
8. Arne May

In Physiology

1. R. Ji
2. Clifford J. Woolf
3. T. Berta
4. Maiken Nedergaard
5. G. Moalem-Taylor
6. P. Austin
7. Jürgen Sandkühler
8. Arne May

Citations in the corpus

• Models and mechanisms of hyperalgesia and allodynia. (2009, neutral): “glycinergic inhibition via the 2 subtype (173).”
• Glia and pain: Is chronic pain a gliopathy? (2013, background): “IL-1b can also be produced by microglia and neurons in the spinal cord [36,51,92].”
• Cellular and Molecular Mechanisms of Pain (2009, neutral): “In this case, the mechanism involves a spinal cord action of prostaglandins (Harvey et al., 2004).”
• Central sensitization: Implications for the diagnosis and treatment of pain (2010, background): “by reducing inhibition [12,103,168,180,165,208,226] or increasing membrane excitability can recruit these normal subthreshold inputs to suprathreshold action potentials, producing profound changes in functional properties [270].”