{'fraction_non_alphanumeric': 0.029565217391304348, 'fraction_numerical': 0.004347826086956522, 'mean_word_length': 6.104938271604938, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Silent synapses in neuromuscular junction development

In the last few years, evidence has been found to suggest that some synaptic contacts become silent but can be functionally recruited before they completely retract during postnatal synapse elimination in muscle. The physiological mechanism of developmental synapse elimination may be better understood by studying this synapse recruitment. This Mini‐Review collects previously published data and new results to propose a molecular mechanism for axonal disconnection. The mechanism is based on protein kinase C (PKC)‐dependent inhibition of acetylcholine (ACh) release. PKC activity may be stimulated by a methoctramine‐sensitive M2‐type muscarinic receptor and by calcium inflow though P/Q‐ and L‐type voltage‐dependent calcium channels. In addition, tropomyosin‐related tyrosine kinase B (trkB) receptor‐mediated brain‐derived neurotrophic factor (BDNF) activity may oppose the PKC‐mediated ACh release depression. Thus, a balance between trkB and muscarinic pathways may contribute to the final functional suppression of some neuromuscular synapses during development. © 2010 Wiley‐Liss, Inc.