scholarly journals All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity

2021 ◽  
Vol 118 (37) ◽  
pp. e2105388118
Author(s):  
Daniel Severin ◽  
Su Z. Hong ◽  
Seung-Eon Roh ◽  
Shiyong Huang ◽  
Jiechao Zhou ◽  
...  
Keyword(s):  
Cortical Plasticity ◽  
Classical Model ◽  
Ocular Dominance ◽  
Pyramidal Cells ◽  
Initial Step ◽  
Monocular Deprivation ◽  
Cortical Circuits ◽  
Ocular Dominance Plasticity ◽  
Layer 2 ◽  
Mouse Visual Cortex

Disinhibition is an obligatory initial step in the remodeling of cortical circuits by sensory experience. Our investigation on disinhibitory mechanisms in the classical model of ocular dominance plasticity uncovered an unexpected form of experience-dependent circuit plasticity. In the layer 2/3 of mouse visual cortex, monocular deprivation triggers a complete, “all-or-none,” elimination of connections from pyramidal cells onto nearby parvalbumin-positive interneurons (Pyr→PV). This binary form of circuit plasticity is unique, as it is transient, local, and discrete. It lasts only 1 d, and it does not manifest as widespread changes in synaptic strength; rather, only about half of local connections are lost, and the remaining ones are not affected in strength. Mechanistically, the deprivation-induced loss of Pyr→PV is contingent on a reduction of the protein neuropentraxin2. Functionally, the loss of Pyr→PV is absolutely necessary for ocular dominance plasticity, a canonical model of deprivation-induced model of cortical remodeling. We surmise, therefore, that this all-or-none loss of local Pyr→PV circuitry gates experience-dependent cortical plasticity.

scholarly journals All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity

2021 ◽  
Author(s):  
Daniel Severin ◽  
Su Z. Hong ◽  
Seung-Eon Roh ◽  
Jiechao Zhou ◽  
Michelle C. D. Bridi ◽  
...  
Keyword(s):  
Critical Period ◽  
Cortical Plasticity ◽  
Classical Model ◽  
Ocular Dominance ◽  
Pyramidal Cells ◽  
Initial Step ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Reversible Loss ◽  
Underlying Mechanisms

ABSTRACTDisinhibition is an obligatory initial step in the remodeling of cortical circuits by sensory experience, yet the underlying mechanisms remain unclear. Our investigation of mechanisms for disinhibition in the classical model of ocular dominance plasticity (ODP) uncovered an unexpected novel form of experience-dependent circuit plasticity. In layer 2/3 of mouse visual cortex monocular deprivation triggers an “all-or-none” elimination of approximately half the connections from local pyramidal cells onto parvalbumin-positive interneurons (Pyr→PV), without affecting the strength of the remaining connections. This loss of Pyr→PV connections is transient, lasting one day only, has a critical period commensurate with the ODP critical period, and is contingent on a reduction of neuropentraxin2 (NPTX2), which normally stabilizes Pyr→PV connections. Bidirectional manipulations of NPTX2 functionality that prevent/promote the elimination Pyr→PV connections also promote/prevent ODP. We surmise, therefore, that this rapid and reversible loss of local Pyr→PV circuitry gates experience-dependent cortical plasticity.

scholarly journals Can ocular dominance plasticity provide a general index to visual plasticity to personalize treatment in amblyopia?

2020 ◽  
Author(s):  
Chunwen Tao ◽  
Zhifen He ◽  
Yiya Chen ◽  
Jiawei Zhou ◽  
Robert F. Hess
Keyword(s):  
Visual Acuity ◽  
Cortical Plasticity ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Homeostatic Plasticity ◽  
Ocular Dominance Plasticity ◽  
Anisometropic Amblyopia ◽  
Occlusion Therapy ◽  
General Index ◽  
Before And After

AbstractPurposeRecently, Lunghi et al showed that amblyopic eye’s visual acuity per se after 2 months of occlusion therapy could be predicted by a homeostatic plasticity, i.e., the temporary shift of ocular dominance observed after a 2-hour monocular deprivation, in children with anisometropic amblyopia(Lunghi et al., 2016). In this study, we assess whether the visual acuity improvement of the amblyopic eye measured after 2 months of occlusion therapy could be predicted by this plasticity.MethodsSeven children (6.86 ± 1.46 years old; SD) with anisometropic amblyopia participated in this study. All patients were newly diagnosed and had no treatment history before participating in our study. They had finished 2 months of refractive adaptation and then received a 4-hour daily fellow eye patching therapy with an opaque patch for a 2-month period. Best-corrected visual acuity of the amblyopic eye was measured before and after the patching therapy. The homeostatic plasticity was assessed by measuring the temporary shift of ocular dominance observed after 2 hours of occlusion for the amblyopic eye before the treatment started. A binocular phase combination paradigm was used for this test.ResultsWe found that there was no significant correlation between the temporary shift of ocular dominance observed after 2 hours of occlusion for the amblyopic eye before the treatment started and the visual acuity gain obtained by the amblyopic eye from 2-month of classical patching therapy. This result involving the short-term patching of the amblyopic eye is consistent with a reanalysis of Lunghi et al’ s data.ConclusionsOcular dominance plasticity does not provide an index of cortical plasticity in the general sense such that it could be used to predict acuity outcomes from longer term classical patching.

scholarly journals Pull-Push Neuromodulation of Cortical Plasticity Enables Rapid Bi-Directional Shifts in Ocular Dominance

2019 ◽  
Author(s):  
Su Z. Hong ◽  
Shiyong Huang ◽  
Daniel Severin ◽  
Alfredo Kirkwood
Keyword(s):  
Cortical Plasticity ◽  
Ocular Dominance ◽  
Long Term Potentiation ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Hebbian Plasticity ◽  
Term Potentiation ◽  
Visual Cortical

SUMMARYNeuromodulatory systems are essential for remodeling glutamatergic connectivity during experience-dependent cortical plasticity. This permissive/enabling function of neuromodulators has been associated with their capacity to facilitate the induction of Hebbian forms of long-term potentiation (LTP) and depression (LTD) by affecting cellular and network excitability. In vitro studies indicate that neuromodulators can also affect the expression of Hebbian plasticity in a pull-push manner: receptors coupled to the G-protein Gs promote the expression of LTP at the expense of LTD, and Gq-coupled receptors promote LTD at the expense of LTD. Here we show that the pull-push mechanism can be recruited in vivo by pairing brief monocular stimulation with pharmacological or chemogenetical activation of Gs- or Gq-coupled receptors to respectively enhance or reduce visual cortical responses. These changes were stable, can be induced in adults after the termination of the critical period for juvenile ocular dominance plasticity, and can rescue deficits induced by prolonged monocular deprivation.

scholarly journals Sleep Slow Oscillations and Spindles encode ocular dominance plasticity and promote its consolidation in adult humans

2021 ◽  
Author(s):  
Danilo Menicucci ◽  
Claudia Lunghi ◽  
Andrea Zaccaro ◽  
Maria Concetta Morrone ◽  
Angelo Gemignani
Keyword(s):  
Cortical Plasticity ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Homeostatic Plasticity ◽  
Ocular Dominance Plasticity ◽  
Slow Oscillations ◽  
Adult Humans ◽  
The Individual ◽  
Visual Cortical

Sleep and plasticity are highly interrelated, as sleep slow oscillations and sleep spindles are associated with consolidation of Hebbian-based processes. However, in adult humans, visual cortical plasticity is mainly sustained by homeostatic mechanisms, for which the role of sleep is still largely unknown. Here we demonstrate that non-REM sleep stabilizes homeostatic plasticity of ocular dominance in adult humans. We found that the effect of short-term monocular deprivation (boost of the deprived eye) was preserved at the morning awakening (>6 hours after deprivation). Subjects exhibiting stronger consolidation had increased sleep spindle density in frontopolar electrodes, suggesting distributed consolidation processes. Crucially, the individual susceptibility to visual homeostatic plasticity was encoded by changes in sleep slow oscillation rate and shape and spindle power in occipital sites, consistent with an early visual cortical site of ocular dominance homeostatic plasticity.

scholarly journals Pull-push neuromodulation of cortical plasticity enables rapid bi-directional shifts in ocular dominance

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Su Z Hong ◽  
Shiyong Huang ◽  
Daniel Severin ◽  
Alfredo Kirkwood
Keyword(s):  
Cortical Plasticity ◽  
Ocular Dominance ◽  
Long Term Potentiation ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Hebbian Plasticity ◽  
Term Potentiation

Neuromodulatory systems are essential for remodeling glutamatergic connectivity during experience-dependent cortical plasticity. This permissive/enabling function of neuromodulators has been associated with their capacity to facilitate the induction of Hebbian forms of long-term potentiation (LTP) and depression (LTD) by affecting cellular and network excitability. In vitro studies indicate that neuromodulators also affect the expression of Hebbian plasticity in a pull-push manner: receptors coupled to the G-protein Gs promote the expression of LTP at the expense of LTD, and Gq-coupled receptors promote LTD at the expense of LTP. Here we show that pull-push mechanisms can be recruited in vivo by pairing brief monocular stimulation with pharmacological or chemogenetical activation of Gs- or Gq-coupled receptors to respectively enhance or reduce neuronal responses in primary visual cortex. These changes were stable, inducible in adults after the termination of the critical period for ocular dominance plasticity, and can rescue deficits induced by prolonged monocular deprivation.

scholarly journals Optical imaging of the intrinsic signal as a measure of cortical plasticity in the mouse

2005 ◽  
Vol 22 (5) ◽  
pp. 685-691 ◽  
Author(s):  
JIANHUA CANG ◽  
VALERY A. KALATSKY ◽  
SIEGRID LÖWEL ◽  
MICHAEL P. STRYKER
Keyword(s):  
Visual Cortex ◽  
Optical Imaging ◽  
Critical Period ◽  
Cortical Plasticity ◽  
Ocular Dominance ◽  
Screening Method ◽  
Intrinsic Signals ◽  
Intrinsic Signal ◽  
The Mean ◽  
Mouse Visual Cortex

The responses of cells in the visual cortex to stimulation of the two eyes changes dramatically following a period of monocular visual deprivation (MD) during a critical period in early life. This phenomenon, referred to as ocular dominance (OD) plasticity, is a widespread model for understanding cortical plasticity. In this study, we designed stimulus patterns and quantification methods to analyze OD in the mouse visual cortex using optical imaging of intrinsic signals. Using periodically drifting bars restricted to the binocular portion of the visual field, we obtained cortical maps for both contralateral (C) and ipsilateral (I) eyes and computed OD maps as (C − I)/(C + I). We defined the OD index (ODI) for individual animals as the mean of the OD map. The ODI obtained from an imaging session of less than 30 min gives reliable measures of OD for both normal and monocularly deprived mice under Nembutal anesthesia. Surprisingly, urethane anesthesia, which yields excellent topographic maps, did not produce consistent OD findings. Normal Nembutal-anesthetized mice have positive ODI (0.22 ± 0.01), confirming a contralateral bias in the binocular zone. For mice monocularly deprived during the critical period, the ODI of the cortex contralateral to the deprived eye shifted negatively towards the nondeprived, ipsilateral eye (ODI after 2-day MD: 0.12 ± 0.02, 4-day: 0.03 ± 0.03, and 6- to 7-day MD: −0.01 ± 0.04). The ODI shift induced by 4-day MD appeared to be near maximal, consistent with previous findings using single-unit recordings. We have thus established optical imaging of intrinsic signals as a fast and reliable screening method to study OD plasticity in the mouse.

Orientation Selectivity Is Reduced by Monocular Deprivation in Combination With PKA Inhibitors

2002 ◽  
Vol 88 (4) ◽  
pp. 1933-1940 ◽  
Author(s):  
Chris J. Beaver ◽  
Quentin S. Fischer ◽  
Qinghua Ji ◽  
Nigel W. Daw
Keyword(s):  
Visual Cortex ◽  
Protein Kinase ◽  
Critical Period ◽  
Ocular Dominance ◽  
Receptive Fields ◽  
Direction Selectivity ◽  
Orientation Selectivity ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Kinase A

We have previously shown that the protein kinase A (PKA) inhibitor, 8-chloroadenosine-3′,5′–monophosphorothioate (Rp-8-Cl-cAMPS), abolishes ocular dominance plasticity in the cat visual cortex. Here we investigate the effect of this inhibitor on orientation selectivity. The inhibitor reduces orientation selectivity in monocularly deprived animals but not in normal animals. In other words, PKA inhibitors by themselves do not affect orientation selectivity, nor does monocular deprivation by itself, but monocular deprivation in combination with a PKA inhibitor does affect orientation selectivity. This result is found for the receptive fields in both deprived and nondeprived eyes. Although there is a tendency for the orientation selectivity in the nondeprived eye to be higher than the orientation selectivity in the deprived eye, the orientation selectivity in both eyes is considerably less than normal. The result is striking in animals at 4 wk of age. The effect of the monocular deprivation on orientation selectivity is reduced at 6 wk of age and absent at 9 wk of age, while the effect on ocular dominance shifts is less changed in agreement with previous results showing that the critical period for orientation/direction selectivity ends earlier than the critical period for ocular dominance. We conclude that closure of one eye in combination with inhibition of PKA reduces orientation selectivity during the period that orientation selectivity is still mutable and that the reduction in orientation selectivity is transferred to the nondeprived eye.

scholarly journals Metabotropic glutamate receptor signaling is required for NMDA receptor-dependent ocular dominance plasticity and LTD in visual cortex

2015 ◽  
Vol 112 (41) ◽  
pp. 12852-12857 ◽  
Author(s):  
Michael S. Sidorov ◽  
Eitan S. Kaplan ◽  
Emily K. Osterweil ◽  
Lothar Lindemann ◽  
Mark F. Bear
Keyword(s):  
Visual Cortex ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Excitatory Synapses ◽  
Ocular Dominance Plasticity ◽  
Metabotropic Glutamate

A feature of early postnatal neocortical development is a transient peak in signaling via metabotropic glutamate receptor 5 (mGluR5). In visual cortex, this change coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD). However, loss of visual responsiveness after MD occurs via mechanisms revealed by the study of long-term depression (LTD) of synaptic transmission, which in layer 4 is induced by acute activation of NMDA receptors (NMDARs) rather than mGluR5. Here we report that chronic postnatal down-regulation of mGluR5 signaling produces coordinated impairments in both NMDAR-dependent LTD in vitro and ocular dominance plasticity in vivo. The data suggest that ongoing mGluR5 signaling during a critical period of postnatal development establishes the biochemical conditions that are permissive for activity-dependent sculpting of excitatory synapses via the mechanism of NMDAR-dependent LTD.

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