Activity-dependent synaptic competition by STDP and its role in critical period plasticity

Neuronal networks are refined through an activity-dependent competition during critical periods of early postnatal development. Recent studies have shown that critical period plasticity is influenced by a number of environmental factors, including drugs that are widely used for the treatment of brain disorders. These findings suggest a new paradigm, where pharmacological treatments can be used to open critical period–like plasticity in the adult brain. The plastic networks can then be modified through rehabilitation or psychotherapy to rewire those abnormally wired during development. This kind of combination of pharmacotherapy with physical or psychological rehabilitation may open a new opportunity for a more efficient recovery of a number of neurological and neuropsychiatric disorders.

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Critical Period for Activity-Dependent Synapse Elimination in Developing Cerebellum

Journal of Neuroscience ◽

10.1523/jneurosci.20-13-04954.2000 ◽

2000 ◽

Vol 20 (13) ◽

pp. 4954-4961 ◽

Cited By ~ 128

Author(s):

Sho Kakizawa ◽

Miwako Yamasaki ◽

Masahiko Watanabe ◽

Masanobu Kano

Keyword(s):

Critical Period ◽

Synapse Elimination ◽

Developing Cerebellum ◽

Activity Dependent

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Neuroplasticity and Psychiatry

Australian & New Zealand Journal of Psychiatry ◽

10.3109/00048679809062718 ◽

1998 ◽

Vol 32 (1) ◽

pp. 119-128 ◽

Cited By ~ 1

Author(s):

Bruce D. Gynther ◽

Mike B. Calford ◽

Pankaj Sah

Keyword(s):

Psychiatric Disorder ◽

Psychiatric Disorders ◽

Neural Development ◽

Critical Period ◽

Clinical Observation ◽

Aggressive Treatment ◽

Long Term Changes ◽

Activity Dependent ◽

The Brain

Objective: There is increasing concern that the course of psychiatric disorders may be affected by parameters such as the duration and intensity of symptoms of initial episodes of illness. As this indicates that abnormal function produces long-term changes within the brain, a review of the neuroscience literature regarding neuroplasticity is warranted. Method: This article is a selective review, focusing in particular on results obtained from physiological experiments assessing plasticity within the mammalian neocortex. The possible relevance of results to psychiatry is discussed. Results: While the most dramatic examples of neuroplasticity occur during a critical period of neural development, neuroplasticity can also occur in adult neocortex. Neuroplasticity appears to be activity-dependent: synaptic pathways that are intensively used may become strengthened, and conversely, there may be depression of transmission in infrequently used pathways. Conclusions: Results from neurophysiological experiments lend support to the clinical observation that the intensity and duration of a psychiatric disorder may adversely alter its long-term course. Rapid aggressive treatment may prevent this from occurring. While pharmacotherapy may reduce the duration and severity of symptoms, it may also have an independent, as yet unknown, effect on neuroplasticity.

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The olfactory critical period is determined by activity-dependent Sema7A/PlxnC1 signaling within glomeruli

eLife ◽

10.7554/elife.65078 ◽

2021 ◽

Vol 10 ◽

Author(s):

Nobuko Inoue ◽

Hirofumi Nishizumi ◽

Rumi Ooyama ◽

Kazutaka Mogi ◽

Katsuhiko Nishimori ◽

...

Keyword(s):

Sensory Neurons ◽

Knockout Mice ◽

Critical Period ◽

Olfactory Sensory Neurons ◽

Early Exposure ◽

Signaling Molecule ◽

Tufted Cells ◽

Olfactory Imprinting ◽

Activity Dependent ◽

Positive Quality

In mice, early exposure to environmental odors affects social behaviors later in life. A signaling molecule, Semaphorin 7A (Sema7A), is induced in the odor-responding olfactory sensory neurons. Plexin C1 (PlxnC1), a receptor for Sema7A, is expressed in mitral/tufted cells, whose dendrite-localization is restricted to the first week after birth. Sema7A/PlxnC1 signaling promotes post-synaptic events and dendrite selection in mitral/tufted cells, resulting in glomerular enlargement that causes an increase in sensitivity to the experienced odor. Neonatal odor experience also induces positive responses to the imprinted odor. Knockout and rescue experiments indicate that oxytocin in neonates is responsible for imposing positive quality on imprinted memory. In the oxytocin knockout mice, the sensitivity to the imprinted odor increases, but positive responses cannot be promoted, indicating that Sema7A/PlxnC1 signaling and oxytocin separately function. These results give new insights into our understanding of olfactory imprinting during the neonatal critical period.

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Arc restores juvenile plasticity in adult mouse visual cortex

10.1101/130880 ◽

2017 ◽

Author(s):

Kyle R. Jenks ◽

Taekeun Kim ◽

Elissa D. Pastuzyn ◽

Hiroyuki Okuno ◽

Andrew V. Taibi ◽

...

Keyword(s):

Visual Cortex ◽

Neural Plasticity ◽

Critical Period ◽

Adult Mouse ◽

Monocular Deprivation ◽

Protein Synthesis Inhibitor ◽

Adult Mice ◽

Mouse Visual Cortex ◽

Activity Dependent

AbstractThe molecular basis for the decline in experience-dependent neural plasticity over age remains poorly understood. In visual cortex, the robust plasticity induced in juvenile mice by brief monocular deprivation (MD) during the critical period is abrogated by genetic deletion of Arc, an activity-dependent regulator of excitatory synaptic modification. Here we report that augmenting Arc expression in adult mice prolongs juvenile-like plasticity in visual cortex, as assessed by recordings of ocular dominance (OD) plasticity in vivo. A distinguishing characteristic of juvenile OD plasticity is the weakening of deprived-eye responses, believed to be accounted for by the mechanisms of homosynaptic long-term depression (LTD). Accordingly, we also found increased LTD in visual cortex of adult mice with augmented Arc expression, and impaired LTD in visual cortex of juvenile mice that lack Arc or have been treated in vivo with a protein synthesis inhibitor. Further, we found that although activity-dependent expression of Arc mRNA does not change with age, expression of Arc protein is maximal during the critical period and declines in adulthood. Finally, we show that acute augmentation of Arc expression in wild type adult mouse visual cortex is sufficient to restore juvenile-like plasticity. Together, our findings suggest a unifying molecular explanation for the age- and activity-dependent modulation of synaptic sensitivity to deprivation.Significance StatementNeuronal plasticity peaks early in life during critical periods and normally declines with age, but the molecular changes that underlie this decline are not fully understood. Using the mouse visual cortex as a model, we found that activity-dependent expression of the neuronal protein Arc peaks early in life, and that loss of activity-dependent Arc expression parallels loss of synaptic plasticity in the visual cortex. Genetic overexpression of Arc prolongs the critical period of visual cortex plasticity and acute viral expression of Arc in adult mice can restore juvenile-like plasticity. These findings provide a mechanism for the loss of excitatory plasticity with age, and suggest that Arc may be an exciting therapeutic target for modulation of the malleability of neuronal circuits.

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An NMDA receptor-dependent mechanism for subcellular segregation of sensory inputs in the tadpole optic tectum

eLife ◽

10.7554/elife.20502 ◽

2016 ◽

Vol 5 ◽

Cited By ~ 5

Author(s):

Ali S Hamodi ◽

Zhenyu Liu ◽

Kara G Pratt

Keyword(s):

Nmda Receptor ◽

Ab Initio ◽

Optic Tectum ◽

Critical Period ◽

Sensory Inputs ◽

Independent Process ◽

Circuit Development ◽

Activity Dependent ◽

Tectal Neuron ◽

Dependent Mechanism

In the vertebrate CNS, afferent sensory inputs are targeted to specific depths or layers of their target neuropil. This patterning exists ab initio, from the very beginning, and therefore has been considered an activity-independent process. However, here we report that, during circuit development, the subcellular segregation of the visual and mechanosensory inputs to specific regions of tectal neuron dendrites in the tadpole optic tectum requires NMDA receptor activity. Blocking NMDARs during the formation of these sensory circuits, or removing the visual set of inputs, leads to less defined segregation, and suggests a correlation-based mechanism in which correlated inputs wire to common regions of dendrites. This can account for how two sets of inputs form synapses onto different regions of the same dendrite. Blocking NMDA receptors during later stages of circuit development did not disrupt segregation, indicating a critical period for activity-dependent shaping of patterns of innervation.

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