Pacinian corpuscle development involves multiple Trk signaling pathways

. 2004 Nov ; 231 (3) : 551-63.

Jazyk angličtina Země Spojené státy americké Médium print

Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem, Research Support, U.S. Gov't, Non-P.H.S., Research Support, U.S. Gov't, P.H.S.

Perzistentní odkaz   https://www.medvik.cz/link/pmid15376326

Grantová podpora
NS 38500 NINDS NIH HHS - United States

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.

Citace poskytuje Crossref.org

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