M. Albuerne et al., Development of Meissner-like and Pacinian sensory corpuscles in the mouse demonstrated with specific markers for corpuscular constituents, ANAT REC, 258(3), 2000, pp. 235-242
The development of Meissner-like and Pacinian corpuscles was studied in mic
e [from postnatal day (Pd) 0 to 42] by using immunohistochemistry for speci
fic corpuscular constituents. The battery of antigens investigated included
PGP 9.5 protein and neurofilaments, as markers for the central axon; S100
protein, vimentin, and p75(LNGFR) protein, to show Schwann-related cells; a
nd epithelial membrane antigen to identify perineurial-related cells. In Me
issner-like corpuscles immunoreactivity (IR) for neuronal markers was found
by Pd7 and later. The lamellar cells of these corpuscles expressed first S
100 protein IR (Pd7 to Pd42), then vimentin IR (Pd12 to Pd42), and transito
ry p75(LNGFR) IR (Pd7 to Pd19-20). Vimentin IR, but not epithelial membrane
antigen, was detected in the capsule-like cells of the Meissner-like corpu
scles. On the other hand, the density of Meissner-like corpuscles progressi
vely increased from Pd0 to Pd19-20. Pacinian corpuscles were identified by
Pd7. From this time to Pd42 the central axon showed IR for neuronal markers
, and the inner core cells were immunoreactive for S100 protein. Moreover,
vimentin IR was detected in the inner core cells by Pd19 and later. Unexpec
tedly, the central axons displayed S100 protein IR (from Pd7 to P28), while
p75(LNGFR) protein IR or epithelial membrane antigen IR were never detecte
d. Taken together, and based on the expression of the assessed antigens alo
ne, the present results suggest that the Meissner-like and the Pacinian cor
puscles in mice become mature around Pd19-Pd28 and Pd20, respectively. Furt
hermore, these results provide a baseline timetable for future studies in t
he normal or altered development of sensory corpuscles in mice since specif
ic sensory corpuscles are functionally associated with different subtypes o
f sensory neurons the development of which is selectively disturbed in gene
tically manipulated mice. Anat Rec 258:235-242, 2000. (C) 2000 Wiley-Liss,
Inc.