Pacinian Corpuscles in a Cervical Chondrocutaneous Remnant: A Case Report and Update of Pacinian Corpuscles.

Cervical chondrocutaneous remnants are congenital, benign, and rare neck masses. We present here for the first time the immunohistochemical profile of Pacinian corpuscles present in cervical chondrocutaneous remnants, removed, and localized in the territory of the second branchial arch from a 5-year-old girl. We have performed immunohistochemistry to analyze these sensory corpuscles using a battery of antibodies including markers for each corpuscle constituent. The central axon was immunoreactive for neurofilaments, neuron-specific enolase, and neural cell adhesion molecule; the Schwann-related cells forming the inner core displayed immunoreactivity for S100 protein, vimentin, and neural cell adhesion molecule; the outer core and the capsule were positive for vimentin, epithelial membrane antigen, and glucose transporter 1. These results are discussed in topographical differences. Moreover, a brief update about the structure, protein composition, and development of Pacinian corpuscles was performed.

Abnormal development of pacinian corpuscles in double trkB;trkC knockout mice.

Pacinian corpuscles depend on either Aalpha or Abeta nerve fibers of the large- and intermediate-sized sensory neurons for the development and maintenance of the structural integrity. These neurons express TrkB and TrkC, two members of the family of signal transducing neurotrophin receptors, and mice lacking TrkB and TrkC lost specific neurons and the sensory corpuscles connected to them. The impact of single or double targeted mutations in trkB and trkC genes in the development of Pacinian corpuscles was investigated in 25-day-old mice using immunohistochemistry and ultrastructural techniques. Single mutations on trkB or trkC genes were without effect on the structure and S100 protein expression, and caused a slight reduction in the number of corpuscles. In mice carrying a double mutation on trkB;trkC genes most of the corpuscles were normal with a reduction of 17% in trkB-/-;trkC+/- mice, and 8% in trkB +/-;trkC -/- mice. Furthermore, a subset of the remaining Pacinian corpuscles (23% in trkB-/-;trkC+/- mice; 3% in trkB+/-;trkC-/- mice) were hypoplasic or atrophic. Present results strongly suggest that the development of a subset of murine Pacinian corpuscles is regulated by the Trk-neurotrophin system, especially TrkB, acting both at neuronal and/or peripheral level. The precise function of each member of this complex in the corpuscular morphogenesis remains to be elucidated, though.