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Updated: Jul 31, 2026

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Monitoring Changes in the Intracellular Calcium Concentration and Synaptic Efficacy in the Mollusc Aplysia
Published on: July 15, 2012
Calcium-dependent maintenance of agrin-induced postsynaptic specializations
L J Megeath1, M T Kirber, C Hopf
1Department of Neuroscience, Brown University, Box 1953, 190 Thayer Street, Providence, RI 02912, USA.
Neuroscience
|November 19, 2003
Summary
Synaptic clusters are maintained by agrin/MuSK-induced calcium fluxes. Blocking these fluxes after cluster formation causes dispersal, revealing distinct pathways for synapse maintenance versus formation.
Area of Science:
- Neuroscience
- Cell Biology
- Synaptic Plasticity
Background:
- Understanding synaptic maintenance is crucial, yet mechanisms remain largely unknown.
- Agrin-induced acetylcholine receptor (AChR) cluster formation requires MuSK activation and calcium fluxes.
Purpose of the Study:
- To investigate the role of intracellular calcium fluxes in maintaining agrin-induced AChR clusters.
- To differentiate signaling pathways involved in synapse formation versus maintenance.
Main Methods:
- Utilizing cultured myotubes and agrin stimulation.
- Manipulating intracellular calcium fluxes via clamping.
- Assessing MuSK and AChR phosphorylation and cluster stability.
- Employing tyrosine phosphatase inhibitors.
Main Results:
- Intracellular calcium fluxes are essential for maintaining AChR clusters.
- Clamping calcium after cluster formation leads to rapid dephosphorylation and dispersal.
- These effects are inhibited by pervanadate.
- Calcium clamping during initial stimulation blocks cluster formation but not phosphorylation.
Conclusions:
- Agrin/MuSK-induced calcium fluxes actively maintain synaptic structures.
- Distinct intracellular signaling pathways regulate synapse formation and maintenance.
- Modulating these pathways offers a novel approach to controlling postsynaptic stability.
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