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Keeping synaptic plasticity plastic
Neuronal synapses in the brain adjust according to shifting demands as we experience the world. This synaptic plasticity forms the basis for critical periods in the visual and somatosensory systems. Greenhill et al. have now found, in mice, a critical period for the development of plasticity itself. At the core is a protein that in its mutant form is associated with schizophrenia. Disrupting this protein's function temporarily during early development caused a failure in brain plasticity in adult mice.
Science, this issue p. 424
Development of the cerebral cortex is influenced by sensory experience during distinct phases of postnatal development known as critical periods. Disruption of experience during a critical period produces neurons that lack specificity for particular stimulus features, such as location in the somatosensory system. Synaptic plasticity is the agent by which sensory experience affects cortical development. Here, we describe, in mice, a developmental critical period that affects plasticity itself. Transient neonatal disruption of signaling via the C-terminal domain of “disrupted in schizophrenia 1” (DISC1)—a molecule implicated in psychiatric disorders—resulted in a lack of long-term potentiation (LTP) (persistent strengthening of synapses) and experience-dependent potentiation in adulthood. Long-term depression (LTD) (selective weakening of specific sets of synapses) and reversal of LTD were present, although impaired, in adolescence and absent in adulthood. These changes may form the basis for the cognitive deficits associated with mutations in DISC1 and the delayed onset of a range of psychiatric symptoms in late adolescence.