Activity-dependent switch from synapse formation to synapse elimination during development of neuromuscular junctions

Herrera, Albert A.; Zeng, Yanhan

doi:10.1023/b:neur.0000020626.29900.fb

Cited by 13 publications

(7 citation statements)

References 150 publications

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“…Hebbian competition between axons refines connectivity and increases specificity ( Purves and Lichtman, 1980 ; Jansen and Fladby, 1990 ; Sanes and Lichtman, 1999 ; Chen and Regehr, 2000 ; Nadal et al, 2016a ). In newborn animals, skeletal muscle cells are innervated by various motor axons ( Ribchester and Barry, 1994 ) but when the competition ends, the NMJs retain only one axon ( Liu et al, 1994 ; Nguyen and Lichtman, 1996 ; Chang and Balice-Gordon, 1997 ; Sanes and Lichtman, 1999 ; Herrera and Zeng, 2003 ; Nelson et al, 2003 ; Wyatt and Balice-Gordon, 2003 ; Buffelli et al, 2004 ).…”

Section: Adenosine Receptors Role During Developmentmentioning

confidence: 99%

Adenosine Receptors in Developing and Adult Mouse Neuromuscular Junctions and Functional Links With Other Metabotropic Receptor Pathways

et al. 2018

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In the last few years, we have studied the presence and involvement in synaptogenesis and mature transmitter release of the adenosine autoreceptors (AR) in the mammalian neuromuscular junction (NMJ). Here, we review and bring together the previously published data to emphasize the relevance of these receptors for developmental axonal competition, synaptic loss and mature NMJ functional modulation. However, in addition to AR, activity-dependent mediators originating from any of the three cells that make the synapse (nerve, muscle, and glial cells) cross the extracellular cleft to generate signals in target metabotropic receptors. Thus, the integrated interpretation of the complementary function of all these receptors is needed. We previously studied, in the NMJ, the links of AR with mAChR and the neurotrophin receptor TrkB in the control of synapse elimination and transmitter release. We conclude that AR cooperate with these receptors through synergistic and antagonistic effects in the developmental synapse elimination process. In the adult NMJ, this cooperation is manifested so as that the functional integrity of a given receptor group depends on the other receptors operating normally (i.e., the functional integrity of mAChR depends on AR operating normally). These observations underlie the relevance of AR in the NMJ function.

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Section: Adenosine Receptors Role During Developmentmentioning

confidence: 99%

Adenosine Receptors in Developing and Adult Mouse Neuromuscular Junctions and Functional Links With Other Metabotropic Receptor Pathways

et al. 2018

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“…Most axonal elimination occurs during the first 2 weeks after birth. At birth, the NMJs are initially polyinnervated but, by the end of the axonal competition, the motor endplates are innervated by a solitary axon (Benoit and Changeux, 1975 ; O’Brien et al, 1978 ; Liu et al, 1994 ; Ribchester and Barry, 1994 ; Nguyen and Lichtman, 1996 ; Chang and Balice-Gordon, 1997 ; Sanes and Lichtman, 1999 ; Herrera and Zeng, 2003 ; Nelson et al, 2003 ; Wyatt and Balice-Gordon, 2003 ; Buffelli et al, 2004 ; Figure 1 ).…”

Section: Developmental Axonal Loss and Synapse Eliminationmentioning

confidence: 99%

Membrane Receptor-Induced Changes of the Protein Kinases A and C Activity May Play a Leading Role in Promoting Developmental Synapse Elimination at the Neuromuscular Junction

Tomàs

García

Lanuza

et al. 2017

Front. Mol. Neurosci.

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Synapses that are overproduced during histogenesis in the nervous system are eventually lost and connectivity is refined. Membrane receptor signaling leads to activity-dependent mutual influence and competition between axons directly or with the involvement of the postsynaptic cell and the associated glial cell/s. Presynaptic muscarinic acetylcholine (ACh) receptors (subtypes mAChR; M1, M2 and M4), adenosine receptors (AR; A1 and A2A) and the tropomyosin-related kinase B receptor (TrkB), among others, all cooperate in synapse elimination. Between these receptors there are several synergistic, antagonic and modulatory relations that clearly affect synapse elimination. Metabotropic receptors converge in a limited repertoire of intracellular effector kinases, particularly serine protein kinases A and C (PKA and PKC), to phosphorylate protein targets and bring about structural and functional changes leading to axon loss. In most cells A1, M1 and TrkB operate mainly by stimulating PKC whereas A2A, M2 and M4 inhibit PKA. We hypothesize that a membrane receptor-induced shifting in the protein kinases A and C activity (inhibition of PKA and/or stimulation of PKC) in some nerve endings may play an important role in promoting developmental synapse elimination at the neuromuscular junction (NMJ). This hypothesis is supported by: (i) the tonic effect (shown by using selective inhibitors) of several membrane receptors that accelerates axon loss between postnatal days P5–P9; (ii) the synergistic, antagonic and modulatory effects (shown by paired inhibition) of the receptors on axonal loss; (iii) the fact that the coupling of these receptors activates/inhibits the intracellular serine kinases; and (iv) the increase of the PKA activity, the reduction of the PKC activity or, in most cases, both situations simultaneously that presumably occurs in all the situations of singly and paired inhibition of the mAChR, AR and TrkB receptors. The use of transgenic animals and various combinations of selective and specific PKA and PKC inhibitors could help to elucidate the role of these kinases in synapse maturation.

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“…On the basis of some of these and other observations, and the competitive nature of nerve and receptor loss, several mechanisms have been postulated to understand the synapse elimination process (Liu et al. ; Nguyen & Lichtman, ; Chang & Balice‐Gordon, ; Sanes & Lichtman, ; Herrera & Zeng, ; Nelson et al. ; Wyatt & Balice‐Gordon, ; Buffelli et al.…”

Section: Pkc Signallingin Developmental Activity‐dependent Synapse Elmentioning

confidence: 99%

Protein kinase C isoforms at the neuromuscular junction: localization and specific roles in neurotransmission and development

et al. 2013

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The protein kinase C family (PKC) regulates a variety of neural functions including neurotransmitter release. The selective activation of a wide range of PKC isoforms in different cells and domains is likely to contribute to the functional diversity of PKC phosphorylating activity. In this review, we describe the isoform localization, phosphorylation function, regulation and signalling of the PKC family at the neuromuscular junction. Data show the involvement of the PKC family in several important functions at the neuromuscular junction and in particular in the maturation of the synapse and the modulation of neurotransmission in the adult.

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Activity-dependent switch from synapse formation to synapse elimination during development of neuromuscular junctions

Cited by 13 publications

References 150 publications

Adenosine Receptors in Developing and Adult Mouse Neuromuscular Junctions and Functional Links With Other Metabotropic Receptor Pathways

Adenosine Receptors in Developing and Adult Mouse Neuromuscular Junctions and Functional Links With Other Metabotropic Receptor Pathways

Membrane Receptor-Induced Changes of the Protein Kinases A and C Activity May Play a Leading Role in Promoting Developmental Synapse Elimination at the Neuromuscular Junction

Protein kinase C isoforms at the neuromuscular junction: localization and specific roles in neurotransmission and development

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