Brain‐derived neurotrophic factor is upregulated in the cervical dorsal root ganglia and spinal cord and contributes to the maintenance of pain from facet joint injury in the rat

@article{Kras2013BrainderivedNF,
  title={Brain‐derived neurotrophic factor is upregulated in the cervical dorsal root ganglia and spinal cord and contributes to the maintenance of pain from facet joint injury in the rat},
  author={Jeffrey V. Kras and Christine L. Weisshaar and Julia C. Quindlen and Beth A. Winkelstein},
  journal={Journal of Neuroscience Research},
  year={2013},
  volume={91}
}
The facet joint is commonly associated with neck and low back pain and is susceptible to loading‐induced injury. Although tensile loading of the cervical facet joint has been associated with inflammation and neuronal hyperexcitability, the mechanisms of joint loading‐induced pain remain unknown. Altered brain‐derived neurotrophic factor (BDNF) levels are associated with a host of painful conditions, but the role of BDNF in loading‐induced joint pain remains undefined. Separate groups of rats… 
View on Wiley
spinepain.seas.upenn.edu
35 Citations
Highly Influential Citations
1
Background Citations
7
Methods Citations
4

35 Citations

Citation Type

Citation Type

Intra-articular nerve growth factor regulates development, but not maintenance, of injury-induced facet joint pain & spinal neuronal hypersensitivity.
Ablating spinal NK1-bearing neurons eliminates the development of pain and reduces spinal neuronal hyperexcitability and inflammation from mechanical joint injury in the rat.
Upregulation of BDNF and NGF in Cervical Intervertebral Discs Exposed to Painful Whole-Body Vibration
TLDR
The increases in BDNF and NGF in the cervical discs after painful vibration are observed in typically aneural regions of the disc, consistent with reports of its hyperinnervation.
Increased Interleukin-1&agr; and Prostaglandin E2 Expression in the Spinal Cord at 1 Day After Painful Facet Joint Injury: Evidence of Early Spinal Inflammation
TLDR
The increased expression of 2 inflammatory markers in the spinal cord at 1 day after painful joint injury suggests that spinal inflammation may contribute to the initiation of pain after cervical facet joint injury.
Brain-derived neurotrophic factor as a driving force behind neuroplasticity in neuropathic and central sensitization pain: a new therapeutic target?
TLDR
This section focuses on combining pharmacotherapy with multimodal rehabilitation for balancing the deleterious and therapeutic effects of BNDF treatment in chronic pain patients, as well as accounting for the complex and biopsychosocial nature of chronic pain.
Early Postoperative Nociceptive Threshold and Production of Brain-Derived Neurotrophic Factor Induced by Plantar Incision Are Not Influenced with Minocycline in a Rat: Role of Spinal Microglia
TLDR
The results suggest that spinal microglia does not contribute substantially to post-incisional nociceptive threshold, and the BDNF overexpression response that may contribute to postoperative hyperalgesia and allodynia is likely derived from other sources.
Intra-articular collagenase in the spinal facet joint induces pain, DRG neuron dysregulation and increased MMP-1 absent evidence of joint destruction
TLDR
The induction of sustained sensitivity and nociception without joint damage may explain the clinical disconnect in which symptomatic joint pain patients present without radiographic evidence of joint destruction.
Pain from intra-articular NGF or joint injury in the rat requires contributions from peptidergic joint afferents
Thrombospondin-4 and excitatory synaptogenesis promote spinal sensitization after painful mechanical joint injury
Spinal Astrocytic Thrombospondin-4 Induced by Excitatory Neuronal Signaling Mediates Pain After Facet Capsule Injury
TLDR
The results suggest that afferent activity early after facet joint injury is critical for the induction of spinal TSP4, and preliminary in vitro experiments suggest that the excitatory signaling molecules ATP and glutamate may stimulate astrocytic T SP4 expression.
...
1
2
3
4
...

References

SHOWING 1-10 OF 63 REFERENCES
Painful facet joint injury induces neuronal stress activation in the DRG: Implications for cellular mechanisms of pain
Joint distraction magnitude is associated with different behavioral outcomes and substance P levels for cervical facet joint loading in the rat.
Inflammatory pain mediated by a phenotypic switch in brain-derived neurotrophic factor-immunoreactive dorsal root ganglion neurons innervating the lumbar facet joints in rats
The Prostaglandin E2 Receptor, EP2, Is Upregulated in the Dorsal Root Ganglion After Painful Cervical Facet Joint Injury in the Rat
TLDR
The transient increase in neuronal EP2 suggests, as in other painful joint conditions, that after joint injury nonneuronal cells may migrate to the DRG, some of which likely express EP2.
Upregulation of brain-derived neurotrophic factor in the sensory pathway by selective motor nerve injury in adult rats
TLDR
The results suggest that increased BDNF expression in intact primary sensory neurons and spinal cord may be an important factor in the induction of neuropathic pain without axotomy of sensory neurons.
The effect of site and type of nerve injury on the expression of brain-derived neurotrophic factor in the dorsal root ganglion and on neuropathic pain behavior
Brain derived neurotrophic factor (BDNF) contributes to the pain hypersensitivity following surgical incision in the rats
TLDR
It is shown that incision induced the segmental upregulation of BDNF in the DRG and spinal cord through somatic afferent nerve transmission, and the upregulated BDNF contributed to the pain hypersensitivity induced by surgical incision.
Metabotropic glutamate receptor-5 and protein kinase C-epsilon increase in dorsal root ganglion neurons and spinal glial activation in an adolescent rat model of painful neck injury.
TLDR
The results suggest that adolescents may have a lower tissue tolerance to induce pain and associated nociceptive response than do adults.
Simulated whiplash modulates expression of the glutamatergic system in the spinal cord suggesting spinal plasticity is associated with painful dynamic cervical facet loading.
TLDR
The results suggest that the spinal glutamatergic system may potentiate the persistent behavioral hypersensitivity that is produced following dynamic whiplash-like joint loading; chronic Whiplash pain may be alleviated by blocking mGluR5 expression and/or enhancing glutamate transport through the neuronal transporter EAAC1.
Contribution of the spinal cord BDNF to the development of neuropathic pain by activation of the NR2B-containing NMDA receptors in rats with spinal nerve ligation
...
1
2
3
4
5
...