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Neuronal spiking leads to increase of Ca2+ in axonal terminals. Presynaptic neurotrophin receptors are Ca2+-dependent. Neurotrophins released by postsynaptic neurons as retrograde messengers influence selectively to previously active axonal terminals. Retrograde influences are effective only during period of increased presynaptic sensitivity to neurotrophins that defines time of delay for neurotrophins that acts as reinforcement. Absence of reinforcement may lead to degeneration of active axonal terminals because it also depends on intracellular Ca2+ concentration. The mechanism presented is very attractive to understand spatial and temporal specificity of associative plasticity.