BDNF as a pain modulator

Merighi, Adalberto; Salio, Chiara; Ghirri, Alessia; Lossi, Laura; Ferrini, Francesco; Betelli, Chiara; Bardoni, Rita

doi:10.1016/j.pneurobio.2008.04.004

Cited by 318 publications

(305 citation statements)

References 257 publications

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“…It adjusts neuron apoptosis, promotes the restoration of the myelin sheath of nerve fibers, and is important in the process of synaptic maturation and plasticity. Furthermore, BDNF effects in injury, inflammatory pain and NP as pain-causing factors in Cornu dorsal medullae spinalis have been confirmed generally (40)(41)(42).…”

Section: B Amentioning

confidence: 85%

Brain-derived neurotrophic factor expression in dorsal root ganglia of a lumbar spinal stenosis model in rats

Liu

Chu

et al. 2013

Molecular Medicine Reports

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Abstract. This study aimed to investigate the expression of brain-derived neurotrophic factor (BDNF) in dorsal root ganglia (DRG) of a rat model of lumbar spinal stenosis (LSS). Adult male rats were divided into the operation and sham operation groups. The operation group was comprised of the rat models of LSS. Walking distance and BDNF expression levels in DRG were measured in the two groups at different time points. The total BDNF protein levels and positive cell mean optical density (MOD) values in the operation group were significantly higher at each time point compared with that of the sham operation and preoperative control groups (P<0.05). The total BDNF protein levels and MOD values following sport in the operation group were significantly higher compared with those prior to sport (P<0.05). In the sham operation group, BDNF protein levels and MOD values before and after sport at each time point showed no significant differences than those of the operation group (P>0.05). Moreover, BDNF protein levels and MOD values in the operation group indicated a negative correlation with walking distance. The present study demonstrated that the expression of BDNF in rat models of LSS increased with time and was associated with a decrease in walking distance. BDNF was therefore important for the process of intermittent claudication caused by LSS.

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Section: B Amentioning

confidence: 85%

Brain-derived neurotrophic factor expression in dorsal root ganglia of a lumbar spinal stenosis model in rats

Liu

Chu

et al. 2013

Molecular Medicine Reports

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“…GDNF is not the only growth factor that intervenes in the modulation of the nociceptive input to the spinal cord, as BDNF is today generally acknowledged to act a pronociceptive factor [88].…”

Section: Expert Opinionmentioning

confidence: 99%

Targeting the glial-derived neurotrophic factor and related molecules for controlling normal and pathologic pain

Merighi

2015

Expert Opinion on Therapeutic Targets

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Introduction: GDNF and its family of ligands (GFLs) have several functions in the nervous system. As a survival factor for dopaminergic neurons, GDNF was used in clinical trials for Parkinson's disease. However, GFLs their receptors are potential targets for new pain-controlling drugs. Such a potential should not be underestimated because molecules with analgesic activities in rodents mostly failed to be effective in translational studies. Areas covered:The circuitry, molecular and cellular mechanisms by which GFLs control nociception, their intervention in inflammatory and neuropathic pain, the problems related to effective GDNF delivery to the brain, the possibility to target the GFL receptor complex rather than its ligands, also by the use of non-peptidyl agonists, are discussed. Expert opinion:In nociceptive pathways, an ideal drug should either: i. Target the release of endogenous GFLs from large dense-cored vesicles (LGVs) by acting e.g. onto the phosphatidylinositol-3-phosphate [PtdIns(3)P] pool, which is sensitive to Ca 2+ modulation; ii. Target the GFL receptor complex. Besides to XIB403, a thiol molecule that enhances GFRα family receptor signaling, existing drugs such as retinoic acid and amitriptyline should be considered for effective targeting of GDNF, at least in neuropathic pain. The approach of pain modeling in experimental animals is discussed.

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“…It has a well documented pronociceptive role in inflammatory and neuropathic pain responses, acting at brain stem-descending pain pathways, including the periaqueductal gray (PAG), 2 rostral ventromedial medulla (RVM), and spinal cord (16,17 High levels of BDNF mRNA and protein have been observed within the PAG and RVM (18,19). A study by Guo et al (20) showed that BDNF in the RVM may have originated from BDNF-containing neurons in the PAG and that BDNF activation of TrkB signaling in the RVM induces descending pain facilitation, suggesting that the signaling cascade of BDNFTrkB receptors in the RVM circuitry plays a critical role in the development of persistent pain after inflammation.…”

mentioning

confidence: 99%

“…Previous studies have shown that persistent inflammation up-regulates BDNF, which decreases the KCC2 function of maintaining the chloride gradient for inhibitory GABA synapses, resulting in impaired GABA inhibition and neuronal hyperexcitability in the nucleus raphe magnus (NRM), which is the major structure of the RVM, contributing to pain sensitization (21). As a pain modulator, BDNF can modulate excitatory glutamatergic and inhibitory GABAergic/glycinergic signals (17,22). The glutamatergic systems in the PAG and RVM have been shown to be significant analgesic targets.…”

mentioning

confidence: 99%

Persistent Inflammation-induced Up-regulation of Brain-derived Neurotrophic Factor (BDNF) Promotes Synaptic Delivery of α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Receptor GluA1 Subunits in Descending Pain Modulatory Circuits

Tao

Chen

Zhou

et al. 2014

Journal of Biological Chemistry

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Background: AMPA-type glutamate receptor-mediated synaptic transmission is enhanced in descending pain modulatory circuits under pain conditions. Results: Epigenetic regulation of BDNF by persistent inflammation triggers AMPA receptor GluA1 phosphorylation. Conclusion: Synaptic delivery of GluA1 in the brain stem is initiated by BDNF/TrKB activation under pain conditions. Significance: We investigate how GluA1 is delivered to synapses to understand the molecular mechanisms underlying pain in descending pain modulatory circuits.

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BDNF as a pain modulator

Cited by 318 publications

References 257 publications

Brain-derived neurotrophic factor expression in dorsal root ganglia of a lumbar spinal stenosis model in rats

Brain-derived neurotrophic factor expression in dorsal root ganglia of a lumbar spinal stenosis model in rats

Targeting the glial-derived neurotrophic factor and related molecules for controlling normal and pathologic pain

Persistent Inflammation-induced Up-regulation of Brain-derived Neurotrophic Factor (BDNF) Promotes Synaptic Delivery of α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Receptor GluA1 Subunits in Descending Pain Modulatory Circuits

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