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ATM controls synaptic function, preventing cognitive alterations. ATM is involved in synaptic vesicles release and endocytosis, GABAergic development, and maintenance of a balanced excitatory/inhibitory (E/I) neuronal transmission. In ATM deficiency conditions, neurons display impaired synaptic plasticity (LTP), defect in the maturation of inhibition, and E/I imbalance. These defects might underlie the neurological symptoms of A-T.
