The dual role of calcium in synaptic plasticity at the motor endplate

Focal blockade of postsynaptic acetylcholine receptors (AChRs) in a small region of the neuromuscular junction may cause long-term synapse elimination at that site. Blockade of the whole junction does not cause synapse loss, indicating that it is the contrast in postsynaptic activity between the blocked and unblocked regions which causes withdrawal of the synaptic terminals. This phenomenon can be explained by the dual role of calcium, both in controlling AChR gene transcription and influencing AChR aggregation. A computational model is provided and the stability of the solutions is confirmed by theoretical analysis and computer simulation.