TY - JOUR
T1 - Adult cortical plasticity depends on an early postnatal critical period
AU - Greenhill, Stuart D.
AU - Juczewski, Konrad
AU - de Haan, Annelies M.
AU - Seaton, Gillian
AU - Fox, Kevin
AU - Hardingham, Neil R.
N1 - This is the author’s version of the work. It is posted here by permission of the AAAS for personal use, not for redistribution. The definitive version was published in Science on Volume 349 Issue 6246 24 July 2015], DOI: 10.1126/science.aaa8481
PY - 2015/7/24
Y1 - 2015/7/24
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84938118006&partnerID=8YFLogxK
U2 - 10.1126/science.aaa8481
DO - 10.1126/science.aaa8481
M3 - Article
C2 - 26206934
AN - SCOPUS:84938118006
SN - 0036-8075
VL - 349
SP - 424
EP - 427
JO - Science
JF - Science
IS - 6246
ER -