Experience-dependent homeostatic synaptic plasticity in neocortex

Whitt, Jessica L.; Petrus, Emily; Lee, Hey Kyoung

doi:10.1016/j.neuropharm.2013.02.016

Cited by 56 publications

(54 citation statements)

References 122 publications

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“…The reduction in excitatory synaptic strength was in contrast to a global increase in the strength of excitatory synapses observed in deprived V1, which may indicate a homeostatic adaptation to increased activity in the spared sensory cortices (Whitt et al, 2013). Therefore, we examined whether the feed-forward TC inputs to A1 are altered cross-modally, and how this impacts A1 neuronal properties in the TC recipient layer 4 (L4).…”

Section: Introductionmentioning

confidence: 94%

Crossmodal Induction of Thalamocortical Potentiation Leads to Enhanced Information Processing in the Auditory Cortex

Petrus

Isaiah

Jones

et al. 2014

Neuron

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107

147

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Summary Sensory systems do not work in isolation; instead they show interactions that are specifically uncovered during sensory loss. To identify and characterize these interactions, we investigated whether visual deprivation leads to functional enhancement in primary auditory cortex (A1). We compared sound-evoked responses of A1 neurons in visually-deprived animals to those from normally-reared animals. Here we show that visual deprivation leads to improved frequency selectivity as well as increased frequency and intensity discrimination performance of A1 neurons. Furthermore, we demonstrate in vitro that in adults, visual deprivation strengthens thalamocortical (TC-) synapses in A1, but not in primary visual cortex (V1). Because deafening potentiated TC-synapses in V1 but not A1, cross-modal TC-potentiation seems to be a general property of adult cortex. Our results suggest that adults retain the capability for cross-modal changes while such capability is absent within a sensory modality. Thus multimodal training paradigms might be beneficial in sensory processing disorders.

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Section: Introductionmentioning

confidence: 94%

Crossmodal Induction of Thalamocortical Potentiation Leads to Enhanced Information Processing in the Auditory Cortex

Petrus

Isaiah

Jones

et al. 2014

Neuron

Self Cite

107

147

View full text Add to dashboard Cite

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“…Structural and functional remodeling of the circuitry takes place through activity-dependent synaptic maturation (Doll and Broadie, 2014; West and Greenberg, 2011). In addition to synaptic pruning, there are changes in synaptic size and strength at individual synapses (Whitt et al, 2014). …”

Section: Neurobiological Framework For Cognitive Function: Pfcmentioning

confidence: 99%

Converging models of schizophrenia – Network alterations of prefrontal cortex underlying cognitive impairments

Sakurai

Gamo

Hikida

et al. 2015

Progress in Neurobiology

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The prefrontal cortex (PFC) and its connections with other brain areas are crucial for cognitive function. Cognitive impairments are one of the core symptoms associated with schizophrenia, and manifest even before the onset of the disorder. Altered neural networks involving PFC contribute to cognitive impairments in schizophrenia. Both genetic and environmental risk factors affect the development of the local circuitry within PFC as well as development of broader brain networks, and make the system vulnerable to further insults during adolescence, leading to the onset of the disorder in young adulthood. Since spared cognitive functions correlate with functional outcome and prognosis, a better understanding of the mechanisms underlying cognitive impairments will have important implications for novel therapeutics for schizophrenia focusing on cognitive functions. Multidisciplinary approaches, from basic neuroscience to clinical studies, are required to link molecules, circuitry, networks, and behavioral phenotypes. Close interactions among such fields by sharing a common language on connectomes, behavioral readouts, and other concepts are crucial for this goal.

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“…These compensatory changes occur across the entire distribution of the cell's miniature postsynaptic current (mPSC) amplitudes by a multiplicative scaling factor. Scaling is typically observed and studied in vitro, but has been described to a lesser extent in vivo in the spinal cord (Gonzalez-Islas and Knogler et al, 2010; and visual system (Desai et al, 2002;Goel et al, 2006;Whitt et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Spontaneous Release Regulates Synaptic Scaling in the Embryonic Spinal Network In Vivo

García-Bereguiaín

González-Islas

Lindsly

et al. 2016

Journal of Neuroscience

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Homeostatic plasticity mechanisms maintain cellular or network spiking activity within a physiologically functional range through compensatory changes in synaptic strength or intrinsic cellular excitability. Synaptic scaling is one form of homeostatic plasticity that is triggered after blockade of spiking or neurotransmission in which the strengths of all synaptic inputs to a cell are multiplicatively scaled upward or downward in a compensatory fashion. We have shown previously that synaptic upscaling could be triggered in chick embryo spinal motoneurons by complete blockade of spiking or GABA A receptor (GABA A R) activation for 2 d in vivo. Here, we alter GABA A R activation in a more physiologically relevant manner by chronically adjusting presynaptic GABA release in vivo using nicotinic modulators or an mGluR2 agonist. Manipulating GABA A R activation in this way triggered scaling in a mechanistically similar manner to scaling induced by complete blockade of GABA A Rs. Remarkably, we find that altering action-potential (AP)-independent spontaneous release was able to fully account for the observed bidirectional scaling, whereas dramatic changes in spiking activity associated with spontaneous network activity had little effect on quantal amplitude. The reliance of scaling on an AP-independent process challenges the plasticity's relatedness to spiking in the living embryonic spinal network. Our findings have implications for the trigger and function of synaptic scaling and suggest that spontaneous release functions to regulate synaptic strength homeostatically in vivo.

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Experience-dependent homeostatic synaptic plasticity in neocortex

Cited by 56 publications

References 122 publications

Crossmodal Induction of Thalamocortical Potentiation Leads to Enhanced Information Processing in the Auditory Cortex

Crossmodal Induction of Thalamocortical Potentiation Leads to Enhanced Information Processing in the Auditory Cortex

Converging models of schizophrenia – Network alterations of prefrontal cortex underlying cognitive impairments

Spontaneous Release Regulates Synaptic Scaling in the Embryonic Spinal Network In Vivo

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