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The development of myelinated nociceptors is dependent upon trks in the trigeminal ganglion.
Acta Histochem. 2004; 106(5):337-43.AH

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.

Authors+Show Affiliations

Department of Oral Function and Anatomy, Biodental Research Center, Okayama University Graduate School of Medicine and Dentistry, Okayama 700, Japan. hiroichi@md.okayama-u.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15530548

Citation

Ichikawa, Hiroyuki, et al. "The Development of Myelinated Nociceptors Is Dependent Upon Trks in the Trigeminal Ganglion." Acta Histochemica, vol. 106, no. 5, 2004, pp. 337-43.
Ichikawa H, Matsuo S, Silos-Santiago I, et al. The development of myelinated nociceptors is dependent upon trks in the trigeminal ganglion. Acta Histochem. 2004;106(5):337-43.
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), 337-43.
Ichikawa H, et al. The Development of Myelinated Nociceptors Is Dependent Upon Trks in the Trigeminal Ganglion. Acta Histochem. 2004;106(5):337-43. PubMed PMID: 15530548.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The development of myelinated nociceptors is dependent upon trks in the trigeminal ganglion. AU - Ichikawa,Hiroyuki, AU - Matsuo,Saburo, AU - Silos-Santiago,Inmaculada, AU - Jacquin,Mark F, AU - Sugimoto,Tomosada, PY - 2004/03/18/received PY - 2004/07/01/revised PY - 2004/07/07/accepted PY - 2004/11/9/pubmed PY - 2005/3/23/medline PY - 2004/11/9/entrez SP - 337 EP - 43 JF - Acta histochemica JO - Acta Histochem. VL - 106 IS - 5 N2 - 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. SN - 0065-1281 UR - https://www.unboundmedicine.com/medline/citation/15530548/The_development_of_myelinated_nociceptors_is_dependent_upon_trks_in_the_trigeminal_ganglion_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0065-1281(04)00071-6 DB - PRIME DP - Unbound Medicine ER -