Expression of mRNA for brain-derived neurotrophic factor in the dorsal root ganglion following peripheral inflammation

Cho, Hee-Jung; Kim, Sang-Yul; Park, Mae-Ja; Kim, Dong–Sun; Kim, Jeong-Ki; Chu, Mi-Young

doi:10.1016/s0006-8993(97)00048-6

Cited by 116 publications

(80 citation statements)

References 26 publications

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“…Previous studies have described BDNF mRNA (Ernfors et al, 1990(Ernfors et al, , 1993Wetmore and Olson, 1995;Apfel et al, 1996;Cho et al, 1997) or protein (Wetmore and Olson, 1995;Zhou and Rush, 1996) in adult rat DRG cells, and two studies have recently reported that some cells expressing BDNF mRNA also express trkA mRNA (Apfel et al, 1996;Cho et al, 1997). We have extended these studies by fully characterizing the expression of both BDNF mRNA and protein in relation to all of the trkexpressing subpopulations of DRG cells.…”

Section: Drg Subgroups That Synthesize Bdnfmentioning

confidence: 69%

“…Many trkA-expressing DRG cells are nociceptive, and increased NGF in inflammation has both acute and chronic effects on pain processing (McMahon, 1996;Woolf, 1996). We have shown that exogenous NGF increases BDNF expression in trkA cells, and Cho et al (1997) have recently shown that similar changes take place after peripheral inflammation. BDNF released from primary afferent terminals may therefore play a key role in chronic pain states by modulating dorsal horn activity in various ways.…”

Section: Upregulation Of Bdnf By Ngf and Its Functional Consequencesmentioning

confidence: 74%

“…BDN F, however, is unusual in being also produced by adult dorsal root ganglion (DRG) cells (Ernfors et al, 1990(Ernfors et al, , 1993Wetmore and Olson, 1995;Apfel al., 1996;Cho et al, 1997), although the role of this BDN F is not known. An autocrine role has been proposed on the basis of studies of single-neuron microcultures (Acheson et al, 1995).…”

Section: Abstract: Brain-derived Neurotrophic Factor; Mrna; Trka; Trmentioning

confidence: 99%

“…Alternatively, BDNF protein has been suggested to be released locally to act in a paracrine manner on trkB cells (Apfel et al, 1996); however, there is little information regarding the dorsal root ganglion (DRG) subtypes that synthesize BDNF. Two studies have recently reported that NGF increases BDNF mRNA in trkA-expressing cells (Apfel et al, 1996;Cho et al, 1997), but it is not known whether trkB or trkC cells synthesize BDNF. It is also not known how the expression of BDNF protein and/or mRNA relates to subgroups of DRG cells defined according to widely used neurochemical criteria (Hunt et al, 1992;Lawson, 1992).…”

Section: Abstract: Brain-derived Neurotrophic Factor; Mrna; Trka; Trmentioning

confidence: 99%

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Nerve Growth Factor Treatment Increases Brain-Derived Neurotrophic Factor Selectively in TrkA-Expressing Dorsal Root Ganglion Cells and in Their Central Terminations within the Spinal Cord

Michael

Averill

Nitkunan³

et al. 1997

J. Neurosci.

485

380

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Using immunocytochemistry and in situ hybridization, we have examined the expression of brain-derived neurotrophic factor (BDNF) and of neurotrophin receptors in dorsal root ganglion cells. In the adult rat, BDNF mRNA and protein were found mainly in the subpopulation of cells that express the nerve growth factor (NGF) receptor trkA and the neuropeptide calcitonin gene-related peptide (CGRP). NGF increased BDNF within the trkA/CGRP cells to the extent that almost 90% of trkA cells contained BDNF mRNA after intrathecal NGF treatment, and 80-90% of BDNF-expressing cells contained trkA. Non-trkA cells that expressed BDNF included some trkC cells and some small cells that labeled with the lectin Griffonia simplicifolia IB4, a marker for cells that do not express trks. However, very few trkB cells expressed either BDNF mRNA or protein, and NGF did not increase BDNF expression in non-trkA cells. BDNF protein was anterogradely transported both peripherally and centrally. The central transport resulted in BDNF immunoreactivity in CGRP containing terminal arbors in the dorsal horn of the spinal cord, and this immunoreactivity was increased by NGF treatment. Electron microscopic analysis revealed that the BDNF immunoreactivity was present in finely myelinated and unmyelinated axons and in axon terminals, where it was most concentrated over dense-cored vesicles.Our data do not support an autocrine or paracrine role for BDNF within normal dorsal root ganglia, but indicate that BDNF may act as an anterograde trophic messenger. NGF levels in the periphery could influence dorsal horn neurons via release of BDNF from primary afferents.

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Section: Drg Subgroups That Synthesize Bdnfmentioning

confidence: 69%

Section: Upregulation Of Bdnf By Ngf and Its Functional Consequencesmentioning

confidence: 74%

Section: Abstract: Brain-derived Neurotrophic Factor; Mrna; Trka; Trmentioning

confidence: 99%

Section: Abstract: Brain-derived Neurotrophic Factor; Mrna; Trka; Trmentioning

confidence: 99%

See 2 more Smart Citations

Nerve Growth Factor Treatment Increases Brain-Derived Neurotrophic Factor Selectively in TrkA-Expressing Dorsal Root Ganglion Cells and in Their Central Terminations within the Spinal Cord

Michael

Averill

Nitkunan³

et al. 1997

J. Neurosci.

485

380

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“…After inflammation, BDNF mRNA is increased in dorsal root ganglion (DRG) neurons in a nerve growth factor (NGF)-dependent fashion (14), in keeping with the up-regulation of BDNF mRNA and protein in these neurons after systemic NGF administration (1). NGF levels increase in inflamed tissue (15) and contributes to basal (16)(17)(18) and stimulusinduced inflammatory hyperalgesia (19).…”

mentioning

confidence: 93%

Neurotrophins: Peripherally and centrally acting modulators of tactile stimulus-induced inflammatory pain hypersensitivity

Mannion

Costigan

Décosterd

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

399

277

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Brain-derived neurotrophic factor (BDNF) is expressed in nociceptive sensory neurons and transported anterogradely to the dorsal horn of the spinal cord where it is located in dense core vesicles in C-fiber terminals. Peripheral inf lammation substantially up-regulates BDNF mRNA and protein in the dorsal root ganglion (DRG) in a nerve growth factor-dependent fashion and results in novel expression of BDNF by DRG neurons with myelinated axons. C-fiber electrical activity also increases BDNF expression in the DRG, and both inf lammation and activity increase full-length TrkB receptor levels in the dorsal horn. Sequestration of endogenous BDNF͞neurotrophin 4 by intraspinal TrkB-Fc fusion protein administration does not, in noninf lamed animals, change basal pain sensitivity nor the mechanical hypersensitivity induced by peripheral capsaicin administration, a measure of C fiber-mediated central sensitization. TrkB-Fc administration also does not modify basal inf lammatory pain hypersensitivity, but does block the progressive hypersensitivity elicited by low-intensity tactile stimulation of inf lamed tissue. BDNF, by virtue of its nerve growth factor regulation in sensory neurons including novel expression in A fibers, has a role as a central modulator of tactile stimulus-induced inf lammatory pain hypersensitivity.

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Distinct expression of TRPM8, TRPA1, and TRPV1 mRNAs in rat primary afferent neurons with aδ/c‐fibers and colocalization with trk receptors

Kobayashi,

Fukuoka,

Obata

et al. 2005

J of Comparative Neurology

688

552

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The transient receptor potential (TRP) superfamily of cation channels contains four temperature-sensitive channels, named TRPV1-4, that are activated by heat stimuli from warm to that in the noxious range. Recently, two other members of this superfamily, TRPA1 and TRPM8, have been cloned and characterized as possible candidates for cold transducers in primary afferent neurons. Using in situ hybridization histochemistry and immunohistochemistry, we characterized the precise distribution of TRPA1, TRPM8, and TRPV1 mRNAs in the rat dorsal root ganglion (DRG) and trigeminal ganglion (TG) neurons. In the DRG, TRPM8 mRNA was not expressed in the TRPV1-expressing neuronal population, whereas TRPA1 mRNA was only seen in some neurons in this population. Both A-fiber and C-fiber neurons expressed TRPM8, whereas TRPV1 was almost exclusively seen in C-fiber neurons. All TRPM8-expressing neurons also expressed TrkA, whereas the expression of TRPV1 and TRPA1 was independent of TrkA expression. None of these three TRP channels were coexpressed with TrkB or TrkC. The TRPM8-expressing neurons were more abundant in the TG compared with the DRG, especially in the mandibular nerve region innervating the tongue. Our data suggest heterogeneity of TRPM8 and TRPA1 expression by subpopulations of primary afferent neurons, which may result in the difference of cold-sensitive primary afferent neurons in sensitivity to chemicals such as menthol and capsaicin and nerve growth factor.

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Expression of mRNA for brain-derived neurotrophic factor in the dorsal root ganglion following peripheral inflammation

Cited by 116 publications

References 26 publications

Nerve Growth Factor Treatment Increases Brain-Derived Neurotrophic Factor Selectively in TrkA-Expressing Dorsal Root Ganglion Cells and in Their Central Terminations within the Spinal Cord

Nerve Growth Factor Treatment Increases Brain-Derived Neurotrophic Factor Selectively in TrkA-Expressing Dorsal Root Ganglion Cells and in Their Central Terminations within the Spinal Cord

Neurotrophins: Peripherally and centrally acting modulators of tactile stimulus-induced inflammatory pain hypersensitivity

Distinct expression of TRPM8, TRPA1, and TRPV1 mRNAs in rat primary afferent neurons with aδ/c‐fibers and colocalization with trk receptors

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