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Abstract:
Memories are assumed to be formed by sets of synapses changing their
structural or functional performance. The efficacy of forming new
memories declines with advancing age, but the synaptic changes
underlying age-induced memory impairment remain poorly understood.
Recently, we found spermidine feeding to specifically suppress
age-dependent impairments in forming olfactory memories, providing a
mean to search for synaptic changes involved in age-dependent memory
impairment. Here, we show that a specific synaptic compartment, the
presynaptic active zone (AZ), increases the size of its ultrastructural
elaboration and releases significantly more synaptic vesicles with
advancing age. These age-induced AZ changes, however, were fully
suppressed by spermidine feeding. A genetically enforced enlargement of
AZ scaffolds (four gene-copies of BRP) impaired memory formation in
young animals. Thus, in the Drosophila nervous system, aging AZs seem to
steer towards the upper limit of their operational range, limiting
synaptic plasticity and contributing to impairment of memory formation.
Spermidine feeding suppresses age-dependent memory impairment by
counteracting these age-dependent changes directly at the synapse.