The development of myelinated nociceptors is dependent upon trks in the trigeminal ganglion

Hiroyuki Ichikawa, Saburo Matsuo, Inmaculada Silos-Santiago, Mark F. Jacquin, Tomosada Sugimoto

Research output: Contribution to journalArticle

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Abstract

Cell size of primary sensory neurons and distribution patterns of neurons that are immunopositive (ip) for VRL-1, a newly cloned capsaicin-receptor homologue, were examined in trigeminal ganglia (TGs) of knockout mice for trkA, trkB or trkC to determine the developmental dependency of myelinated nociceptors on expression of the genes. The number of TG neurons was strongly decreased in the knockout mice as compared to wildtype and heterozygous mice (82%, 39%, and 48% reduction for trkA, trkB and trkC, respectively). The absence of trkA and trkC reduced the number of TG neurons in all cell-size ranges. The number of medium-sized and large TG neurons was decreased in trkB-knockout mice, whereas that of small TG neurons was barely affected by trkB deficiency. TG contained abundant VRL-1-ip neurons in wildtype and heterozygous mice; 9% of TG neurons exhibited immunopositivity. In trkA-knockout mice, VRL-1-ip neurons almost disappeared (1% of TG neurons were VRL-1-ip). However, 13% and 9% of TG neurons in trkB- and trkC-knockout mice, respectively, were immunostained for the ion channel protein. In trkC-knockout mice, the proportion of large VRL-1-ip neurons decreased whereas that of small and medium-sized VRL-1-ip neurons increased. In addition, immunohistochemistry of the protein gene product 9.5 (PGP 9.5) demonstrated that trkA deficiency caused a marked reduction of varicose endings in the epithelium of the palatal mucosa. Loss of trkC diminished the number of PGP 9.5-ip varicose fibers in the deep layer of mucosal connective tissue of the palate. In tooth pulp, PGP 9.5-ip nerve fibers were absent in trkA-knockout mice but abundant in trkB- and trkC-knockout mice. The present study suggests that the development of myelinated nociceptors is dependent on trkA and trkC but not on trkB.

Original languageEnglish
Pages (from-to)337-343
Number of pages7
JournalActa Histochemica
Volume106
Issue number5
DOIs
Publication statusPublished - Nov 25 2004

Fingerprint

Trigeminal Ganglion
Nociceptors
Neurons
Knockout Mice
Cell Size
Mucous Membrane
Proteins
TRPV Cation Channels
Palate
Sensory Receptor Cells
Ion Channels
Nerve Fibers
Connective Tissue
Tooth
Epithelium

Keywords

  • Free nerve endings
  • Mutant mice
  • Palate
  • Tooth pulp
  • Trigeminal ganglion
  • Trk
  • VRL-1

ASJC Scopus subject areas

  • Cell Biology

Cite this

Ichikawa, H., Matsuo, S., Silos-Santiago, I., Jacquin, M. F., & Sugimoto, T. (2004). The development of myelinated nociceptors is dependent upon trks in the trigeminal ganglion. Acta Histochemica, 106(5), 337-343. https://doi.org/10.1016/j.acthis.2004.07.003

The development of myelinated nociceptors is dependent upon trks in the trigeminal ganglion. / Ichikawa, Hiroyuki; Matsuo, Saburo; Silos-Santiago, Inmaculada; Jacquin, Mark F.; Sugimoto, Tomosada.

In: Acta Histochemica, Vol. 106, No. 5, 25.11.2004, p. 337-343.

Research output: Contribution to journalArticle

Ichikawa, H, Matsuo, S, Silos-Santiago, I, Jacquin, MF & Sugimoto, T 2004, 'The development of myelinated nociceptors is dependent upon trks in the trigeminal ganglion', Acta Histochemica, vol. 106, no. 5, pp. 337-343. https://doi.org/10.1016/j.acthis.2004.07.003
Ichikawa, Hiroyuki ; Matsuo, Saburo ; Silos-Santiago, Inmaculada ; Jacquin, Mark F. ; Sugimoto, Tomosada. / The development of myelinated nociceptors is dependent upon trks in the trigeminal ganglion. In: Acta Histochemica. 2004 ; Vol. 106, No. 5. pp. 337-343.
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abstract = "Cell size of primary sensory neurons and distribution patterns of neurons that are immunopositive (ip) for VRL-1, a newly cloned capsaicin-receptor homologue, were examined in trigeminal ganglia (TGs) of knockout mice for trkA, trkB or trkC to determine the developmental dependency of myelinated nociceptors on expression of the genes. The number of TG neurons was strongly decreased in the knockout mice as compared to wildtype and heterozygous mice (82{\%}, 39{\%}, and 48{\%} reduction for trkA, trkB and trkC, respectively). The absence of trkA and trkC reduced the number of TG neurons in all cell-size ranges. The number of medium-sized and large TG neurons was decreased in trkB-knockout mice, whereas that of small TG neurons was barely affected by trkB deficiency. TG contained abundant VRL-1-ip neurons in wildtype and heterozygous mice; 9{\%} of TG neurons exhibited immunopositivity. In trkA-knockout mice, VRL-1-ip neurons almost disappeared (1{\%} of TG neurons were VRL-1-ip). However, 13{\%} and 9{\%} of TG neurons in trkB- and trkC-knockout mice, respectively, were immunostained for the ion channel protein. In trkC-knockout mice, the proportion of large VRL-1-ip neurons decreased whereas that of small and medium-sized VRL-1-ip neurons increased. In addition, immunohistochemistry of the protein gene product 9.5 (PGP 9.5) demonstrated that trkA deficiency caused a marked reduction of varicose endings in the epithelium of the palatal mucosa. Loss of trkC diminished the number of PGP 9.5-ip varicose fibers in the deep layer of mucosal connective tissue of the palate. In tooth pulp, PGP 9.5-ip nerve fibers were absent in trkA-knockout mice but abundant in trkB- and trkC-knockout mice. The present study suggests that the development of myelinated nociceptors is dependent on trkA and trkC but not on trkB.",
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