scholarly journals Distinct Laminar Requirements for NMDA Receptors in Experience-Dependent Visual Cortical Plasticity

2019 ◽  
Vol 30 (4) ◽  
pp. 2555-2572 ◽  
Author(s):  
Ming-fai Fong ◽  
Peter Sb Finnie ◽  
Taekeun Kim ◽  
Aurore Thomazeau ◽  
Eitan S Kaplan ◽  
...  
Keyword(s):  
Cortical Plasticity ◽  
Visual Stimulation ◽  
Cortical Layer ◽  
Monocular Deprivation ◽  
Dependent Plasticity ◽  
Synaptic Modification ◽  
Layer 4 ◽  
Nmdar Activation ◽  
Visual Cortical

Abstract Primary visual cortex (V1) is the locus of numerous forms of experience-dependent plasticity. Restricting visual stimulation to one eye at a time has revealed that many such forms of plasticity are eye-specific, indicating that synaptic modification occurs prior to binocular integration of thalamocortical inputs. A common feature of these forms of plasticity is the requirement for NMDA receptor (NMDAR) activation in V1. We therefore hypothesized that NMDARs in cortical layer 4 (L4), which receives the densest thalamocortical input, would be necessary for all forms of NMDAR-dependent and input-specific V1 plasticity. We tested this hypothesis in awake mice using a genetic approach to selectively delete NMDARs from L4 principal cells. We found, unexpectedly, that both stimulus-selective response potentiation and potentiation of open-eye responses following monocular deprivation (MD) persist in the absence of L4 NMDARs. In contrast, MD-driven depression of deprived-eye responses was impaired in mice lacking L4 NMDARs, as was L4 long-term depression in V1 slices. Our findings reveal a crucial requirement for L4 NMDARs in visual cortical synaptic depression, and a surprisingly negligible role for them in cortical response potentiation. These results demonstrate that NMDARs within distinct cellular subpopulations support different forms of experience-dependent plasticity.

scholarly journals NMDA Receptor Antagonists Reveal Age-Dependent Differences in the Properties of Visual Cortical Plasticity

2008 ◽  
Vol 100 (4) ◽  
pp. 1936-1948 ◽  
Author(s):  
Jacqueline de Marchena ◽  
Adam C. Roberts ◽  
Paul G. Middlebrooks ◽  
Vera Valakh ◽  
Koji Yashiro ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Nmda Receptor ◽  
Cortical Plasticity ◽  
Long Term Potentiation ◽  
Underlying Mechanism ◽  
Developmental Shift ◽  
Term Potentiation ◽  
Nmdar Activation ◽  
Visual Cortical

The suggestion that NMDA receptor (NMDAR)-dependent plasticity is subunit specific, with NR2B-types required for long-term depression (LTD) and NR2A-types critical for the induction of long-term potentiation (LTP), has generated much attention and considerable debate. By investigating the suggested subunit-specific roles of NMDARs in the mouse primary visual cortex over development, we report several important findings that clarify the roles of NMDAR subtypes in synaptic plasticity. We observed that LTD was not attenuated by application of ifenprodil, an NR2B-type antagonist, or NVP-AAM007, a less selective NR2A-type antagonist. However, we were surprised that NVP-AAM007 completely blocked adult LTP (postnatal day (P) 45–90), while only modestly affecting juvenile LTP (P21-28). To assess whether this developmental transition reflected an increasing role for NR2A-type receptors with maturity, we characterized the specificity of NVP-AAM007. We found not only that NVP-AAM007 lacks discernable subunit specificity but also that the effects of NVP-AAM077 on LTP could be mimicked using subsaturating concentrations of APV, a global NMDAR antagonist. These results indicate that the effects of NVP-AAM077 on synaptic plasticity are largely explained by nonspecific blockade of NMDARs. Moreover our findings are the first to reveal a developmental increase in the sensitivity of LTP to NMDAR antagonism. We suggest that discrepant reports describing the effect of NVP-AAM077 on LTP may be partially explained by this developmental shift in the properties of LTP. These results indicate that the degree of NMDAR activation required for LTP increases with development, providing insight into a novel underlying mechanism governing the properties of synaptic plasticity.

scholarly journals How the mechanisms of long-term synaptic potentiation and depression serve experience-dependent plasticity in primary visual cortex

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130284 ◽  
Author(s):  
Sam F. Cooke ◽  
Mark F. Bear
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Visual Learning ◽  
Excitatory Input ◽  
Monocular Deprivation ◽  
Hebbian Plasticity ◽  
Circuit Components ◽  
Cortical Synapses ◽  
Visual Cortical

Donald Hebb chose visual learning in primary visual cortex (V1) of the rodent to exemplify his theories of how the brain stores information through long-lasting homosynaptic plasticity. Here, we revisit V1 to consider roles for bidirectional ‘Hebbian’ plasticity in the modification of vision through experience. First, we discuss the consequences of monocular deprivation (MD) in the mouse, which have been studied by many laboratories over many years, and the evidence that synaptic depression of excitatory input from the thalamus is a primary contributor to the loss of visual cortical responsiveness to stimuli viewed through the deprived eye. Second, we describe a less studied, but no less interesting form of plasticity in the visual cortex known as stimulus-selective response potentiation (SRP). SRP results in increases in the response of V1 to a visual stimulus through repeated viewing and bears all the hallmarks of perceptual learning. We describe evidence implicating an important role for potentiation of thalamo-cortical synapses in SRP. In addition, we present new data indicating that there are some features of this form of plasticity that cannot be fully accounted for by such feed-forward Hebbian plasticity, suggesting contributions from intra-cortical circuit components.

scholarly journals Early cross-modal interactions and adult human visual cortical plasticity revealed by binocular rivalry

2015 ◽  
Author(s):  
Claudia Lunghi
Keyword(s):  
Visual Cortex ◽  
Binocular Rivalry ◽  
Visual Processing ◽  
Cortical Plasticity ◽  
Monocular Deprivation ◽  
Homeostatic Plasticity ◽  
Multisensory Perception ◽  
Modal Interactions ◽  
Early Visual Cortex ◽  
Visual Cortical

In this research binocular rivalry is used as a tool to investigate different aspects of visual and multisensory perception. Several experiments presented here demonstrated that touch specifically interacts with vision during binocular rivalry and that the interaction likely occurs at early stages of visual processing, probably V1 or V2. Another line of research also presented here demonstrated that human adult visual cortex retains an unexpected high degree of experience-dependent plasticity by showing that a brief period of monocular deprivation produced important perceptual consequences on the dynamics of binocular rivalry, reflecting a homeostatic plasticity. In summary, this work shows that binocular rivalry is a powerful tool to investigate different aspects of visual perception and can be used to reveal unexpected properties of early visual cortex.

A Calcium-Based Simple Model of Multiple Spike Interactions in Spike-Timing-Dependent Plasticity

2013 ◽  
Vol 25 (7) ◽  
pp. 1853-1869 ◽  
Author(s):  
Takumi Uramoto ◽  
Hiroyuki Torikai
Keyword(s):  
Synaptic Weight ◽  
Spike Timing ◽  
State Variables ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Synaptic Modification ◽  
Proposed Model ◽  
Layer 2 ◽  
Visual Cortical ◽  
Cortical Slices

Spike-timing-dependent plasticity (STDP) is a form of synaptic modification that depends on the relative timings of presynaptic and postsynaptic spikes. In this letter, we proposed a calcium-based simple STDP model, described by an ordinary differential equation having only three state variables: one represents the density of intracellular calcium, one represents a fraction of open state NMDARs, and one represents the synaptic weight. We shown that in spite of its simplicity, the model can reproduce the properties of the plasticity that have been experimentally measured in various brain areas (e.g., layer 2/3 and 5 visual cortical slices, hippocampal cultures, and layer 2/3 somatosensory cortical slices) with respect to various patterns of presynaptic and postsynaptic spikes. In addition, comparisons with other STDP models are made, and the significance and advantages of the proposed model are discussed.

Reactivation of visual cortical plasticity by NEP1-40 from early monocular deprivation in adult rats

2011 ◽  
Vol 494 (3) ◽  
pp. 196-201 ◽  
Author(s):  
Yulin Luo ◽  
Xiaoying Wu ◽  
Shuangzhen Liu ◽  
Kuanshu Li
Keyword(s):  
Cortical Plasticity ◽  
Monocular Deprivation ◽  
Adult Rats ◽  
Visual Cortical

scholarly journals A Computational Model of the Effect of Short−Term Monocular Deprivation on Binocular Rivalry in the Context of Amblyopia

2021 ◽  
Author(s):  
Norman Seeliger ◽  
Jochen Triesch
Keyword(s):  
Binocular Rivalry ◽  
Cortical Plasticity ◽  
Monocular Deprivation ◽  
Homeostatic Plasticity ◽  
Short Term ◽  
Successful Prediction ◽  
Inhibitory Plasticity ◽  
Underlying Mechanisms ◽  
Visual Cortical ◽  
Vision Therapy

Treatments for amblyopia focus on vision therapy and patching of one eye. Predicting the success of these methods remains difficult, however. Recent research has used binocular rivalry to monitor visual cortical plasticity during occlusion therapy, leading to a successful prediction of the recovery rate of the amblyopic eye. The underlying mechanisms and their relation to neural homeostatic plasticity are not known. Here we propose a spiking neural network to explain the effect of shortterm monocular deprivation on binocular rivalry. The model reproduces perceptual switches as observed experimentally. When one eye is occluded, inhibitory plasticity changes the balance between the eyes and leads to longer dominance periods for the eye that has been deprived. The model suggests that homeostatic inhibitory plasticity is a critical component of the observed effects and might play an important role in the recovery from amblyopia.

scholarly journals Activation of somatostatin interneurons by nicotinic modulator Lypd6 enhances plasticity and functional recovery in the adult mouse visual cortex

2017 ◽  
Author(s):  
Masato Sadahiro ◽  
Michael P. Demars ◽  
Poromendro Burman ◽  
Priscilla Yevoo ◽  
Andreas Zimmer ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Functional Recovery ◽  
Critical Period ◽  
Cortical Plasticity ◽  
Monocular Deprivation ◽  
Adult Brain ◽  
Clinical Issue ◽  
Dependent Plasticity ◽  
Excitatory Neurons ◽  
Interneuron Activity

AbstractThe limitation of plasticity in the adult brain impedes functional recovery later in life from brain injury or disease. This pressing clinical issue may be resolved by enhancing plasticity in the adult brain. One strategy for triggering robust plasticity in adulthood is to reproduce one of the hallmark physiological events of experience-dependent plasticity observed during the juvenile critical period – rapidly reduce the activity of parvalbumin (PV)-expressing interneurons and disinhibit local excitatory neurons. This may be achieved through enhancement of local inhibitory inputs, particularly those of somatostatin (SST)-expressing interneurons. However, to date the means for manipulating SST interneurons for enhancing cortical plasticity in the adult brain are not known. We show that SST interneuron-selective overexpression of Lypd6, an endogenous nicotinic signaling modulator, enhances ocular dominance plasticity in the adult primary visual cortex (V1). Lypd6 overexpression mediates a rapid experience-dependent increase in the visually evoked activity of SST interneurons as well as a simultaneous reduction in PV interneuron activity and disinhibition of excitatory neurons. Recapitulating this transient activation of SST interneurons using chemogenetics similarly enhanced V1 plasticity. Notably, we show that SST-selective Lypd6 overexpression restores visual acuity in amblyopic mice that underwent early long-term monocular deprivation. Our data in both male and female mice reveal selective modulation of SST interneurons and a putative downstream circuit mechanism as an effective method for enhancing experience-dependent cortical plasticity as well as functional recovery in adulthood.Significance StatementThe decline of cortical plasticity after closure of juvenile critical period consolidates neural circuits and behavior, but this limits functional recovery from brain diseases and dysfunctions in later life. Here we show that activation of cortical SST interneurons by Lypd6, an endogenous modulator of nicotinic acetylcholine receptors (nAChRs), enhances experience-dependent plasticity and recovery from amblyopia in adulthood. This manipulation triggers rapid reduction of PV interneuron activity and disinhibition of excitatory neurons, which are known hallmarks of cortical plasticity during juvenile critical periods. Our study demonstrates modulation of SST interneurons by Lypd6 to achieve robust levels of cortical plasticity in the adult brain and may provide promising targets for restoring brain function in the event of brain trauma or disease.

scholarly journals Transcriptomics of critical period of visual cortical plasticity in mice

2015 ◽  
Vol 112 (26) ◽  
pp. 8094-8099 ◽  
Author(s):  
Jamie Benoit ◽  
Albert E. Ayoub ◽  
Pasko Rakic
Keyword(s):  
Gene Expression ◽  
Critical Period ◽  
Cortical Plasticity ◽  
Differentially Expressed Gene ◽  
Prenatal Development ◽  
Mature Stage ◽  
Dependent Plasticity ◽  
Genetic Constraints ◽  
Visual Cortical ◽  
Activity Dependent

In contrast to the prenatal development of the cerebral cortex, when cell production, migration, and layer formation dominate, development after birth involves more subtle processes, such as activity-dependent plasticity that includes refinement of synaptic connectivity by its stabilization and elimination. In the present study, we use RNA-seq with high spatial resolution to examine differential gene expression across layers 2/3, 4, 5, and 6 of the mouse visual cortex before the onset of the critical period of plasticity [postnatal day 5 (P5)], at its peak (P26), and at the mature stage (P180) and compare it with the prefrontal association area. We find that, although genes involved in early developmental events such as cell division, neuronal migration, and axon guidance are still prominent at P5, their expression largely terminates by P26, when synaptic plasticity and associated signaling pathways become enriched. Unexpectedly, the gene expression profile was similar in both areas at this age, suggesting that activity-dependent plasticity between visual and association cortices are subject to the same genetic constraints. Although gene expression changes follow similar paths until P26, we have identified 30 regionally enriched genes that are prominent during the critical period. At P180, we identified several hundred differentially expressed gene isoforms despite subsiding levels of gene expression differences. This result indicates that, once genetic developmental programs cease, the remaining morphogenetic processes may depend on posttranslational events.

Contribution of Individual Spikes in Burst-Induced Long-Term Synaptic Modification

2006 ◽  
Vol 95 (3) ◽  
pp. 1620-1629 ◽  
Author(s):  
Robert C. Froemke ◽  
Ishan A. Tsay ◽  
Mohamad Raad ◽  
John D. Long ◽  
Yang Dan
Keyword(s):  
High Frequency ◽  
Spike Timing ◽  
Relative Timing ◽  
Short Term ◽  
Burst Frequency ◽  
Synaptic Modification ◽  
Visual Cortical ◽  
Cortical Slices ◽  
Dependent Interaction

Long-term synaptic modification depends on the relative timing of individual pre- and postsynaptic spikes, but the rules governing the effects of multispike bursts remain to be fully understood. In particular, some studies suggest that the spike timing dependence of synaptic modification breaks down with high-frequency bursts. In this study, we characterized the effects of pre- and postsynaptic bursts on long-term modification of layer 2/3 synapses in visual cortical slices from young rats. We found that, while pairing-induced synaptic modification depends on the burst frequency, this dependence can be explained in terms of the timing of individual pre- and postsynaptic spikes. Later spikes in each burst are less effective in synaptic modification, but spike efficacy is regulated differently in pre- and postsynaptic bursts. Presynaptically, spike efficacy is progressively weakened, in parallel with short-term synaptic depression. Postsynaptically, spike efficacy is suppressed to a lesser extent, and it depends on postsynaptic potassium channel activation. Such timing-dependent interaction among multiple spikes can account for synaptic modifications induced by a variety of spike trains, including the frequency-dependent transition from depression to potentiation induced by a postsynaptic burst preceding a presynaptic burst.

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