Developmental dependency of Merkel endings on trks in the palate

Brain Res Mol Brain Res. 2001 Mar 31;88(1-2):171-5. doi: 10.1016/s0169-328x(01)00035-3.

Abstract

Immunohistochemistry for protein gene product 9.5 was performed on Merkel cells in the palate of wildtype and knockout mice for trkA, trkB or trkC. In wildtype mice, numerous Merkel cells were observed at the top of anterior four rugae. In the posterior four rugae, Merkel cells were fewer and mostly located at the base of rugae. In knockout mice for trkA, trkB and trkC, Merkel cells at the top of rugae mostly disappeared although those at the base of rugae remained unchanged. Therefore, the number of Merkel cells in anterior four rugae decreased. In posterior four rugae, however, the number of Merkel cells in the mutant mice was similar to that for wildtype mice. Immunohistochemistry for S100 also demonstrated that the loss of genes for trkA, trkB and trkC caused the absence of the immunoreactive innervation of Merkel cells. The normal development of Merkel endings at the top of palatal rugae is probably dependent on trkA, trkB and trkC.

MeSH terms

  • Animals
  • Gene Expression Regulation, Developmental*
  • Merkel Cells / chemistry
  • Merkel Cells / physiology*
  • Mice
  • Mice, Knockout
  • Palate / innervation
  • Receptor, trkA / genetics
  • Receptor, trkB / genetics
  • Receptor, trkC / genetics
  • Receptors, Nerve Growth Factor / genetics*
  • S100 Proteins / analysis
  • Thiolester Hydrolases / analysis
  • Ubiquitin Thiolesterase

Substances

  • Receptors, Nerve Growth Factor
  • S100 Proteins
  • S100A1 protein
  • Receptor, trkA
  • Receptor, trkB
  • Receptor, trkC
  • Thiolester Hydrolases
  • Ubiquitin Thiolesterase