Reorganization of Synaptic Inputs to Developing Skeletal Muscle Fibres

Vrbová, Gerta; Mb, Lowrie; J, Evers

doi:10.1002/9780470513675.ch9

Cited by 4 publications

(4 citation statements)

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“…What could be the mechanism activated by the high [Ca 2+ ] i ? It is plausible that a calcium-activated neutral protease (CANP) present in nerve endings could contribute [ 83 ]. A greater increase of Ca 2+ concentration in smaller terminals would be expected, because of their surface-to-volume ratio and the collegiate activity of several VGCC.…”

Section: Discussionmentioning

confidence: 99%

Involvement of the Voltage-Gated Calcium Channels L- P/Q- and N-Types in Synapse Elimination During Neuromuscular Junction Development

et al. 2022

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During the nervous system development, synapses are initially overproduced. In the neuromuscular junction (NMJ) however, competition between several motor nerve terminals and the synapses they made ends with the maturation of only one axon. The competitive signaling between axons is mediated by the differential activity-dependent release of the neurotransmitter ACh, co-transmitters, and neurotrophic factors. A multiple metabotropic receptor-driven downstream balance between PKA and PKC isoforms modulates the phosphorylation of targets involved in transmitter release and nerve terminal stability. Previously, we observed in the weakest endings on the polyinnervated NMJ that M1 mAChR receptors reduce ACh release through the PKC pathway coupled to an excess of Ca2+ inflow through P/Q- N- and L-type voltage-gated calcium channels (VGCC). This signaling would contribute to the elimination of this nerve terminal. Here, we investigate the involvement of the P/Q-, N-, and L-subtype channels in transgenic B6.Cg-Tg (Thy1-YFP)16-Jrs/J mice during synapse elimination. Then, the axon number and postsynaptic receptor cluster morphologic maturation were evaluated. The results show that both L- and P/Q-type VGCC (but not the N-type) are equally involved in synapse elimination. Their normal function favors supernumerary axonal loss by jointly enhancing intracellular calcium [Ca2+]i. The block of these VGCCs or [Ca2+]i i sequestration results in the same delay of axonal loss as the cPKCβI and nPKCε isoform block or PKA activation. The specific block of the muscle cell’s contraction with μ-conotoxin GIIIB also delays synapse maturation, and thus, a retrograde influence from the postsynaptic site regulating the presynaptic CaV1.3 may contribute to the synapse elimination.

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Section: Discussionmentioning

confidence: 99%

Involvement of the Voltage-Gated Calcium Channels L- P/Q- and N-Types in Synapse Elimination During Neuromuscular Junction Development

et al. 2022

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“…• πρωτεάσες όπως η CANP (Calcium Activated Neutral Protease) (Swanson & Vrbova 1987, Sazontova 1999) και η καλπαϊνη, που προκαλούν διάσπαση νευροϊνιδίων, αποπολυμερισμό των μικροσωληναρίων και τελικά λύση του κυτταροσκελετού (O'Brien 1984, Vrbova 1988, Connold 1986, Navarrette & Vrbova 1993, Lo Pachin 1997.…”

Section: ο μηχανισμός του κυτταρικού θανάτουunclassified

“…Ακόμη, πολλές μελέτες απέδειξαν, ότι μετά από αξονότμηση σε επίμυες νεογνικής ηλικίας, οι νευρώνες που εκφυλίζονται και πεθαίνουν είναι κυρίως εκείνοι που νευρώνουν ταχέως συστελλόμενες κινητικές μονάδες. Έτσι η μείωση των κινητικών νευρώνων που καταλήγουν στον ΜΕΔ ή τον πρόσθιο κνημιαίο είναι πολύ μεγαλύτερη από την αντίστοιχη στον υποκνημίδιο (Nicolopoulos -Stournaras 1983, Lowrie et al, 1982& 1984& 1987& 1988, Albani et al, 1988.…”

Section: αξονότμηση -η επίδραση στους μυςunclassified

“…Έτσι ο μυς μετατρέπεται σε βραδέως συστελλόμενο. Τα αποτελέσματα της παρούσας μελέτης έδειξαν ότι η αξονότμηση επηρέασε τον ΜΕΔ πολύ περισσότερο από τον υποκνημίδιο, όπως ακριβώς ανέφεραν και άλλοι ερευνητές, που μελέτησαν ιστολογικά ευρήματα (Lowrie et al, 1988) και καταγραφές ισομετρικής συστολής (Lowrie & Vrbova 1984). Επίσης αναφέρθηκε ότι μετά από απονεύρωση, αναστέλλεται σημαντικά, η αύξηση στην ταχύτητα συστολής κατά τη φυσιολογική ανάπτυξη (Navarrete & Vrbova 1993).…”

Section: συζητησηunclassified

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