Involvement of neurotrophin-3 (NT-3) in the functional elimination of synaptic contacts during neuromuscular development

• Published in: Neuroscience letters 2010-04, Vol.473 (2), p.141-145
• Main Authors: Garcia, Neus, Santafé, Manel M., Tomàs, Marta, Lanuza, Maria A., Besalduch, Nuria, Tomàs, Josep
• Format: Article
• Language: English
• Subjects: Acetylcholine - metabolism; ACh release; Animals; Biological and medical sciences; Evoked Potentials; Excitatory Postsynaptic Potentials; Fundamental and applied biological sciences. Psychology; In Vitro Techniques; Mice; Motor Endplate - growth & development; Motor Endplate - physiology; Motor nerve terminals; Nerve Growth Factors - metabolism; Nerve Growth Factors - pharmacology; Neuromuscular junction; Neuromuscular Junction - growth & development; Neuromuscular Junction - physiology; Neurotrophins; Presynaptic Terminals - physiology; Receptor, trkC - metabolism; Synapse elimination; Synapses - physiology; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2010.02.040

Confocal immunohistochemistry shows that neurotrophin-3 (NT-3) and its receptor tropomyosin-related tyrosin kinase C (trkC) are present in both neonatal (P6) and adult (P45) mouse motor nerve terminals in neuromuscular junctions (NMJ) colocalized with several synaptic proteins. NT-3 incubation (1–3 h, in the range 10–200 ng/ml) does not change the size of the evoked and spontaneous endplate potentials at P45. However, NT-3 (1 h, 100 ng/ml) strongly potentiates evoked ACh release from the weak (70%) and the strong (50%) axonal inputs on dually innervated postnatal endplates (P6) but not in the most developed postnatal singly innervated synapses at P6. The present results indicate that NT-3 has a role in the developmental mechanism that eliminates redundant synapses though it cannot modulate synaptic transmission locally as the NMJ matures.