We recently demonstrated the utility of quantifying spontaneous pain in mice via the blinded coding of facial expressions. As the majority of preclinical pain research is in fact performed in the laboratory rat, we attempted to modify the scale for use in this species. We present herein the Rat Grimace Scale, and show its reliability,…
Molecular Pain Template
Write in a clean editor, then format for Molecular Pain in one click — DocuGuru applies the official SAGE template with author–year references and exports a submission-ready PDF plus the editable LaTeX source. Free to start.
About the Molecular Pain format
Molecular Pain is a peer-reviewed journal published by SAGE, covering Pain Mechanisms and Treatments, Neuropeptides and Animal Physiology, Ion channel regulation and function.
| Publisher | SAGE |
|---|---|
| Reference style | Author–year (Harvard) Author–year — (Smith, 2023) in the text Smith, A., Jones, B. and Lee, C. (2023) 'A representative article title', Molecular Pain, 12(3), pp. 45–58.
Formats any DOI in Molecular Pain style. No sign-up. |
| Publishes research in | Pain Mechanisms and Treatments Neuropeptides and Animal Physiology Ion channel regulation and function Ion Channels and Receptors Neuroscience and Neuropharmacology Research |
| ISSN | 1744-8069 |
| Citation impact (2-yr) | 2.16 |
| h-index | 116 |
| i10-index | 1,249 |
| Total citations | 67,092 |
| Article processing charge | $2,500 |
| Open access | Yes |
| Top institutions publishing here | University of Toronto |
| Journal website | www.molecularpain.com |
| You get | A submission-ready PDF and the editable LaTeX source — ready to submit. |
Papers published in Molecular Pain per year
Citation impact of Molecular Pain by publication year
Citations each year’s papers have accumulated so far — the most recent years are still building up.
Most-cited papers in Molecular Pain
Accumulating evidence over last several years indicates an important role of microglial cells in the pathogenesis of neuropathic pain. Signal transduction in microglia under chronic pain states has begun to be revealed. We will review the evidence that p38 MAPK is activated in spinal microglia after nerve injury and contributes importantly to neuropathic pain development…
Prostaglandin E2 (PGE2) and prostaglandin I2 (PGI2) are major inflammatory mediators that play important roles in pain sensation and hyperalgesia. The role of their receptors (EP and IP, respectively) in inflammation has been well documented, although the EP receptor subtypes involved in this process and the underlying cellular mechanisms remain to be elucidated. The capsaicin…
BACKGROUND: The measurement of mechanosensitivity is a key method for the study of pain in animal models. This is often accomplished with the use of von Frey filaments in an up-down testing paradigm. The up-down method described by Chaplan et al. (J Neurosci Methods 53:55-63, 1994) for mechanosensitivity testing in rodents remains one of the…
BACKGROUND: Safe and effective treatment for chronic inflammatory and neuropathic pain remains a key unmet medical need for many patients. The recent discovery and description of the transient receptor potential family of receptors including TRPV1 and TRPA1 has provided a number of potential new therapeutic targets for treating chronic pain. Recent reports have suggested that…