Evidence map›Paper›PMID 38314104›Full record

ReviewNeurobiology of pain (Cambridge, Mass.)

A review of dorsal root ganglia and primary sensory neuron plasticity mediating inflammatory and chronic neuropathic pain.

Kyeongran Jang, Sandra M Garraway

Open access · goldAbstract readReview
In one paragraph

Review in Neurobiology of pain (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
18.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Channels (Austin, Tex.) · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Shaping the Action Potential in Dorsal Root and Trigeminal Ganglia Neurons: Relevance to Pain Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Review
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Kyeongran JangDepartment of Cell Biology, Emory University, School of Medicine, Atlanta, GA, 30322, USA.
Sandra M GarrawayDepartment of Cell Biology, Emory University, School of Medicine, Atlanta, GA, 30322, USA.
Emory University · US

Funding

Examining the roles A-delta LTMRs and BDNF signaling play in neuropathic pain after SCIR01NS102850 · NINDS · EMORY UNIVERSITY · PI GARRAWAY, SANDRA M. · 2018 to 2022
$1.9M
Peripheral BDNF drives primary afferent hyperexcitability and pain hypersensitivityR21NS116665 · NINDS · EMORY UNIVERSITY · PI GARRAWAY, SANDRA M. · 2020 to 2020
$425k
NINDS NIH HHS R01 NS102850NINDS NIH HHS R21 NS116665
6 · The paper itself

Abstract

Pain is a sensory state resulting from complex integration of peripheral nociceptive inputs and central processing. Pain consists of adaptive pain that is acute and beneficial for healing and maladaptive pain that is often persistent and pathological. Pain is indeed heterogeneous, and can be expressed as nociceptive, inflammatory, or neuropathic in nature. Neuropathic pain is an example of maladaptive pain that occurs after spinal cord injury (SCI), which triggers a wide range of neural plasticity. The nociceptive processing that underlies pain hypersensitivity is well-studied in the spinal cord. However, recent investigations show maladaptive plasticity that leads to pain, including neuropathic pain after SCI, also exists at peripheral sites, such as the dorsal root ganglia (DRG), which contains the cell bodies of sensory neurons. This review discusses the important role DRGs play in nociceptive processing that underlies inflammatory and neuropathic pain. Specifically, it highlights nociceptor hyperexcitability as critical to increased pain states. Furthermore, it reviews prior literature on glutamate and glutamate receptors, voltage-gated sodium channels (VGSC), and brain-derived neurotrophic factor (BDNF) signaling in the DRG as important contributors to inflammatory and neuropathic pain. We previously reviewed BDNF's role as a bidirectional neuromodulator of spinal plasticity. Here, we shift focus to the periphery and discuss BDNF-TrkB expression on nociceptors, non-nociceptor sensory neurons, and non-neuronal cells in the periphery as a potential contributor to induction and persistence of pain after SCI. Overall, this review presents a comprehensive evaluation of large bodies of work that individually focus on pain, DRG, BDNF, and SCI, to understand their interaction in nociceptive processing.

Indexed as

BDNFDorsal root gangliaNociceptorsPainSpinal cord injuryTrkB

Identifiers

PMID38314104
PMCPMC10837099
OpenAlexW4391058689

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.