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Pacinian corpuscle development involves multiple Trk signaling pathways
Author(s) -
Šedý J.,
Szeder V.,
Walro J.M.,
Ren Z.G.,
Naňka O.,
Tessarollo L.,
SieberBlum M.,
Grim M.,
Kucera J.
Publication year - 2004
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20156
Subject(s) - trk receptor , tropomyosin receptor kinase b , tropomyosin receptor kinase a , neurotrophin , tropomyosin receptor kinase c , biology , nerve growth factor , neurotrophin 3 , receptor , low affinity nerve growth factor receptor , neurotrophic factors , neuroscience , endocrinology , brain derived neurotrophic factor , medicine , growth factor , genetics , platelet derived growth factor receptor
The development of crural Pacinian corpuscles was explored in neonatal mutant mice lacking nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), neurotrophin‐3 (NT3) or neurotrophin‐4 (NT4), or their cognate Trk receptors. Deficits of the corpuscles and their afferents were greatest in NT3 , less in BDNF , and least in NT4 null mice. Deletion of NGF or p75 NTR genes had little or no impact. No Pacinian corpuscles were present in NT3;BDNF and NT3;NT4 double or NT3;BDNF;NT4 triple null mice. Deficits were larger in NT3 than TrkC mutants and were comparable to deficits observed in TrkB or TrkA mutants. Afferents of all corpuscles coexpressed TrkA and TrkB receptors, and some afferents coexpressed all three Trk receptors. Our results suggest that multiple neurotrophins, in particular NT3, regulate the density of crural Pacinian corpuscles, most likely by regulating the survival of sensory neurons. In addition, NT3/TrkB and/or NT3/TrkA signaling plays a greater role than NT3/TrkC signaling in afferents to developing Pacinian corpuscles. Developmental Dynamics 231:551–563, 2004. © 2004 Wiley‐Liss, Inc.