scholarly journals Synaptic plasticity onto inhibitory neurons as a mechanism for ocular dominance plasticity

2018 ◽  
Author(s):  
Jacopo Bono ◽  
Claudia Clopath
Keyword(s):  
Synaptic Plasticity ◽  
Critical Period ◽  
Ocular Dominance ◽  
Visual Deprivation ◽  
Inhibitory Neurons ◽  
Cortical Circuits ◽  
Ocular Dominance Plasticity ◽  
Opening And Closing ◽  
Recent Experimental Work ◽  
Cortical Maturation

AbstractOcular dominance plasticity is a well-documented phenomenon allowing us to study properties of cortical maturation. Understanding this maturation might be an important step towards unravelling how cortical circuits function. However, it is still not fully understood which mechanisms are responsible for the opening and closing of the critical period for ocular dominance and how changes in cortical responsiveness arise after visual deprivation. In this article, we present a theory of ocular dominance plasticity. Following recent experimental work, we propose a framework where a reduction in inhibition is necessary for ocular dominance plasticity in both juvenile and adult animals. In this framework, two ingredients are crucial to observe ocular dominance shifts: a sufficient level of inhibition as well as excitatory-to-inhibitory synaptic plasticity. In our model, the former is responsible for the opening of the critical period, while the latter limits the plasticity in adult animals. Finally, we also provide a possible explanation for the variability in ocular dominance shifts observed in individual neurons and for the counter-intuitive shifts towards the closed eye.

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 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 Non-cell autonomous OTX2 homeoprotein regulates visual cortex plasticity through Gadd45

2017 ◽  
Author(s):  
Jessica Apulei ◽  
Namsuk Kim ◽  
Damien Testa ◽  
Jérôme Ribot ◽  
David Morizet ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Ocular Dominance ◽  
Regulation Of Transcription ◽  
Gene Promoters ◽  
Ocular Dominance Plasticity ◽  
Mouse Cerebral Cortex ◽  
Parvalbumin Interneuron ◽  
Adult Plasticity ◽  
Juvenile Mouse

AbstractThe non-cell autonomous transfer of OTX2 homeoprotein transcription factor into juvenile mouse cerebral cortex regulates parvalbumin interneuron maturation and critical period timing. By analyzing gene expression in primary visual cortex of wild-type and Otx2+/GFP mice at plastic and non-plastic ages, we identified several putative genes implicated in Otx2-dependent visual cortex plasticity for ocular dominance. Cortical OTX2 infusion in juvenile mice induced Gadd45b/g expression through direct regulation of transcription. Intriguingly, a reverse effect was found in the adult, where reducing cortical OTX2 resulted in Gadd45b/g up-regulation. Viral expression of Gadd45b in adult visual cortex directly induced ocular dominance plasticity with concomitant changes in MeCP2 foci within parvalbumin interneurons and in methylation states of several plasticity gene promoters, suggesting epigenetic regulation. This interaction provides a molecular mechanism for OTX2 to trigger critical period plasticity yet suppress adult plasticity.

scholarly journals Progressive maturation of silent synapses governs the duration of a critical period

2015 ◽  
Vol 112 (24) ◽  
pp. E3131-E3140 ◽  
Author(s):  
Xiaojie Huang ◽  
Sophia K. Stodieck ◽  
Bianka Goetze ◽  
Lei Cui ◽  
Man Ho Wong ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Neural Circuit ◽  
Ocular Dominance ◽  
Critical Periods ◽  
Ocular Dominance Plasticity ◽  
Silent Synapses ◽  
Synapse Maturation ◽  
Silent Synapse ◽  
Visual Cortical

During critical periods, all cortical neural circuits are refined to optimize their functional properties. The prevailing notion is that the balance between excitation and inhibition determines the onset and closure of critical periods. In contrast, we show that maturation of silent glutamatergic synapses onto principal neurons was sufficient to govern the duration of the critical period for ocular dominance plasticity in the visual cortex of mice. Specifically, postsynaptic density protein-95 (PSD-95) was absolutely required for experience-dependent maturation of silent synapses, and its absence before the onset of critical periods resulted in lifelong juvenile ocular dominance plasticity. Loss of PSD-95 in the visual cortex after the closure of the critical period reinstated silent synapses, resulting in reopening of juvenile-like ocular dominance plasticity. Additionally, silent synapse-based ocular dominance plasticity was largely independent of the inhibitory tone, whose developmental maturation was independent of PSD-95. Moreover, glutamatergic synaptic transmission onto parvalbumin-positive interneurons was unaltered in PSD-95 KO mice. These findings reveal not only that PSD-95–dependent silent synapse maturation in visual cortical principal neurons terminates the critical period for ocular dominance plasticity but also indicate that, in general, once silent synapses are consolidated in any neural circuit, initial experience-dependent functional optimization and critical periods end.

scholarly journals Loss of P2Y12 Has Behavioral Effects in the Adult Mouse

2021 ◽  
Vol 22 (4) ◽  
pp. 1868
Author(s):  
Rebecca L. Lowery ◽  
Monique S. Mendes ◽  
Brandon T. Sanders ◽  
Allison J. Murphy ◽  
Brendan S. Whitelaw ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Ex Vivo ◽  
Purinergic Receptor ◽  
Ocular Dominance ◽  
Developmental Time ◽  
Brain Regions ◽  
Ocular Dominance Plasticity ◽  
Early Form ◽  
Adult Mice ◽  
Molecular Signals

While microglia have been established as critical mediators of synaptic plasticity, the molecular signals underlying this process are still being uncovered. Increasing evidence suggests that microglia utilize these signals in a temporally and regionally heterogeneous manner. Subsequently, it is necessary to understand the conditions under which different molecular signals are employed by microglia to mediate the physiological process of synaptic remodeling in development and adulthood. While the microglial purinergic receptor P2Y12 is required for ocular dominance plasticity, an adolescent form of experience-dependent plasticity, it remains unknown whether P2Y12 functions in other forms of plasticity at different developmental time points or in different brain regions. Using a combination of ex vivo characterization and behavioral testing, we examined how the loss of P2Y12 affects developmental processes and behavioral performance in adulthood in mice. We found P2Y12 was not required for an early form of plasticity in the developing visual thalamus and did not affect microglial migration into barrels in the developing somatosensory cortex. In adult mice, however, the loss of P2Y12 resulted in alterations in recognition and social memory, as well as anxiety-like behaviors, suggesting that while P2Y12 is not a universal regulator of synaptic plasticity, the loss of P2Y12 is sufficient to cause functional defects.

scholarly journals Light reintroduction after dark exposure reactivates plasticity in adults via perisynaptic activation of MMP-9

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Sachiko Murase ◽  
Crystal L Lantz ◽  
Elizabeth M Quinlan
Keyword(s):  
Critical Period ◽  
Adult Mouse ◽  
Ocular Dominance ◽  
Visual Deprivation ◽  
Monocular Deprivation ◽  
Genetic Ablation ◽  
Dark Exposure ◽  
Cortical Synapses ◽  
Mouse Visual Cortex ◽  
Metalloproteinase 9

The sensitivity of ocular dominance to regulation by monocular deprivation is the canonical model of plasticity confined to a critical period. However, we have previously shown that visual deprivation through dark exposure (DE) reactivates critical period plasticity in adults. Previous work assumed that the elimination of visual input was sufficient to enhance plasticity in the adult mouse visual cortex. In contrast, here we show that light reintroduction (LRx) after DE is responsible for the reactivation of plasticity. LRx triggers degradation of the ECM, which is blocked by pharmacological inhibition or genetic ablation of matrix metalloproteinase-9 (MMP-9). LRx induces an increase in MMP-9 activity that is perisynaptic and enriched at thalamo-cortical synapses. The reactivation of plasticity by LRx is absent in Mmp9−/− mice, and is rescued by hyaluronidase, an enzyme that degrades core ECM components. Thus, the LRx-induced increase in MMP-9 removes constraints on structural and functional plasticity in the mature cortex.

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