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Formation of a full complement of cranial proprioceptors requires multiple neurotrophins
Author(s) -
Fan Guoping,
Copray Sjef,
Huang Eric J.,
Jones Kevin,
Yan Qiao,
Walro Jon,
Jaenisch Rudolf,
Kucera Jan
Publication year - 2000
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/(sici)1097-0177(200006)218:2<359::aid-dvdy9>3.0.co;2-l
Subject(s) - tropomyosin receptor kinase b , neurotrophin 3 , tropomyosin receptor kinase c , neurotrophin , biology , brain derived neurotrophic factor , neuroscience , neurotrophic factors , microbiology and biotechnology , anatomy , endocrinology , medicine , receptor , genetics , growth factor , platelet derived growth factor receptor
Inactivation of neurotrophin‐3 (NT3) completely blocks the development of limb proprioceptive neurons and their end organs, the muscle spindles. We examined whether cranial proprioceptive neurons of the trigeminal mesencephalic nucleus (TMN) require NT3, brain‐derived neurotrophic factor (BDNF) or neurotrophin‐4 (NT4) for their development. Complements of TMN neurons and masticatory muscle spindles were decreased by 62% in NT3 null mutants, 33% in BDNF null mutants, and 10% in NT4 null mutant mice at birth. The extent of proprioceptive deficiencies differed among different masticatory muscles, particularly in NT3 null mice. Masticatory muscles of embryonic mice heterozygous for the NT3 lacZneo or BDNF lacZ reporter genes expressed both NT3 and BDNF, consistent with target‐derived neurotrophin support of TMN neurons. Although more than 90% of TMN neurons expressed TrkB as well as TrkC receptor proteins by immunocytochemistry in wild‐type newborns, TrkC or TrkB null mice exhibited only partial proprioceptive deficiencies similar to those present in NT3 or BDNF;NT4 null mice. Thus, in terms of the survival outcome, two main subpopulations of TMN neurons may exist during embryogenesis, one dependent on TrkC/NT3 functioning and the other utilizing TrkB/BDNF signaling. The differential dependence of TMN neurons on neurotrophins may reflect differential accessibility of the neurons to limiting amounts of NT3, BDNF, or NT4 in target tissues, especially if the tissue distribution or levels of BDNF, NT3, and NT4 were dynamically regulated both spatially and temporally. Dev Dyn;218:359–370. © 2000 Wiley‐Liss, Inc.