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Synaptic plasticity, which refers to long-term changes in the efficiency of synaptic transmission in the form of potentiation and depression, is thought to be a cellular mechanism of learning and memory. Long-term potentiation and depression can be induced under a variety of experimental conditions using different induction protocols. One such example is a protocol that follows Hebb’s rule, where induction of plasticity requires paired activation of a pre- and postsynaptic neuron that occur within a narrow temporal window relative to each other. Such plasticity is called homosynaptic plasticity because the same (homo-, Greek prefix meaning “same, identical”) synapses that participated in the induction of plasticity undergo long-term changes. However, as numerous experiments have shown, synapses that were inactive during the induction of plasticity also undergo long-term changes. This process has been termed heterosynaptic (hetero – “other, different”) plasticity in mammalian studies. Historically, however, the term heterosynaptic plasticity first appeared in studies of mollusks, where plastic changes in synaptic transmission were caused by a combination of stimulation of “weak” and “strong” synaptic inputs. As was later shown, the potentiating effect of stimulating the “strong” input in this case was associated with the release of neuromodulators, primarily serotonin. This type of plasticity was later demonstrated in mammals, where it was termed modulatory plasticity. The review considers different types of heterosynaptic plasticity, cellular and molecular mechanisms of its induction and maintenance, and explains the reasons for some terminological confusion related to this phenomenon in the literature.