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Blocking p75 NTR receptors alters polyinnervationz of neuromuscular synapses during development
Author(s) -
Garcia Neus,
Tomàs Marta,
Santafe Manel M.,
Lanuza Maria A.,
Besalduch Nuria,
Tomàs Josep
Publication year - 2011
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22620
Subject(s) - postsynaptic potential , synapse , neuromuscular junction , acetylcholine receptor , long term potentiation , receptor , synaptogenesis , biology , neuroscience , microbiology and biotechnology , chemistry , endocrinology , medicine , biochemistry
High‐resolution immunohistochemistry shows that the receptor protein p75 NTR is present in the nerve terminal, muscle cell, and glial Schwann cell at the neuromuscular junction (NMJ) of postnatal rats (P4–P6) during the synapse elimination period. Blocking the receptor with the antibody anti‐p75‐192‐IgG (1–5 μg/ml, 1 hr) results in reduced endplate potentials (EPPs) in mono‐ and polyinnervated synapses ex vivo, but the mean number of functional inputs per NMJ does not change for as long as 3 hr. Incubation with exogenous brain‐derived neurotrophic factor (BDNF) for 1 hr (50 nM) resulted in a significant increase in the size of the EPPs in all nerve terminals, and preincubation with anti‐p75‐192‐IgG prevented this potentiation. Long exposure (24 hr) in vivo of the NMJs to the antibody anti‐p75‐192‐IgG (1–2 μg/ml) results in a delay of postnatal synapse elimination and even some regrowth of previously withdrawn axons, but also in some acceleration of the morphologic maturation of the postsynaptic nicotinic acetylcholine receptor (nAChR) clusters. The results indicate that p75 NTR is involved in both ACh release and axonal retraction during postnatal axonal competition and synapse elimination. © 2011 Wiley‐Liss, Inc.