Since it is believed that changes in synaptic efficacy underlie memory formation, understanding the cellular mechanisms involved in synaptic plasticity induction and maintenance, can provide new insights into brain function. The induction of synaptic plasticity leads to the input-specific activation of synapses followed by the capture of plasticity-related proteins (PRPs) necessary for the maintenance of plasticity. We have shown that synapses can either cooperate or compete depending on the availability of PRPs. We are interested in understanding how PRPs are captured at activated synapses and the rules that determine whether synapses engage in synaptic cooperation or competition. We have shown that activity-dependent regulation of actin dynamics can capture PRPs in an input-specific manner and we are now addressing the impact of this activity-dependent regulation of actin cytoskeleton in spine morphology, using advanced opto-physiological approaches. What is the contribution of synaptic cooperation and competition to memory formation? To tackle this, we took advantage of a well-characterized circuitry, the thalamic and cortical inputs to the amygdala nuclei. We found that thalamic and cortical synapses can cooperate, providing the first evidence that synaptic cooperation is a general mechanism in synaptic plasticity. We aim to take this question further and test, at the behavioural level, whether synaptic cooperation plays a role in auditory discrimination learning.