The neuromuscular synapse plays a relay function that requires a homeostatic control. This control adapts the neurotransmitter release to the post-synaptic excitability, resulting in a unity synaptic gain (one post-synaptic action potential for one pre-synaptic action potential). For this control process, the post-synaptic cell evaluates the synaptic efficacy and exercises a retrograde feedback on the pre-synaptic terminal. Our work focuses on the postsynaptic sensors that evaluate the synaptic efficacy. We have previously shown (Ouanounou et al. eLife 2016;5:e12190) that postsynaptic calcium signaling reports distinctly the occurrence of the pre- and postsynaptic events, and that this dual detection is used to adjust the neurotransmitter release to a level matching the postsynaptic excitability. Here we confirm and refine the calcium mechanism of the sensor of the synaptic efficacy. We show that in addition to the detection of activities, the postsynaptic sensor precisely reports the synaptic strength. Contrary to the common belief, we discovered that this operation is not done by the quantification of the postsynaptic potential amplitude, masked by the action potential, but of the repolarization kinetics. We show that the sub-synaptic calcium build up, due to the nicotinic receptor permeability to calcium, strongly depends on repolarization kinetics and perfectly encodes the ratio between the synaptic conductance and the postsynaptic input conductance. This signal is used to balance homeostatic synaptic plasticity and to set the synaptic strength ratio around 2.3 in our experimental model.