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.

scholarly journals MEF2C and HDAC5 regulate Egr1 and Arc genes to increase dendritic spine density and complexity in early enriched environment

2020 ◽  
Vol 4 (3) ◽  
Author(s):  
Shu Juan Puang ◽  
Bavani Elanggovan ◽  
Tendy Ching ◽  
Judy C.G. Sng
Keyword(s):  
Transcription Factor ◽  
Dendritic Spine ◽  
Critical Period ◽  
Environmental Enrichment ◽  
Cortical Plasticity ◽  
Postnatal Life ◽  
Spine Density ◽  
Dendritic Spine Density ◽  
Visual Cortical ◽  
Dendritic Complexity

Abstract We investigated the effects of environmental enrichment during critical period of early postnatal life and how it interplays with the epigenome to affect experience-dependent visual cortical plasticity. Mice raised in an EE from birth to during CP have increased spine density and dendritic complexity in the visual cortex. EE upregulates synaptic plasticity genes, Arc and Egr1, and a transcription factor MEF2C. We also observed an increase in MEF2C binding to the promoters of Arc and Egr1. In addition, pups raised in EE show a reduction in HDAC5 and its binding to promoters of Mef2c, Arc and Egr1 genes. With an overexpression of Mef2c, neurite outgrowth increased in complexity. Our results suggest a possible underlying molecular mechanism of EE, acting through MEF2C and HDAC5, which drive Arc and Egr1. This could lead to the observed increased dendritic spine density and complexity induced by early EE.

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.

Nerve growth factor (NGF) uptake and transport following injection in the developing rat visual cortex

1994 ◽  
Vol 11 (6) ◽  
pp. 1093-1102 ◽  
Author(s):  
Luciano Domenici ◽  
Gigliola Fontanesi ◽  
Antonio Cattaneo ◽  
Paola Bagnoli ◽  
Lamberto Maffei
Keyword(s):  
Visual Cortex ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Critical Period ◽  
Cortical Plasticity ◽  
Ocular Dominance ◽  
Occipital Cortex ◽  
Nerve Growth ◽  
Visual Cortical ◽  
Uptake And Transport

AbstractRecent investigations have shown that cortical nerve growth factor (NGF) infusions during the critical period inhibit ocular-dominance plasticity in the binocular portion of the rat visual cortex. The mechanisms underlying the effects of NGF on visual cortical plasticity are still unclear. To investigate whether during normal development intracortical and/or extracortical cells possess uptake/transport mechanisms for the neurotrophin, we injected 125I-NGF into the occipital cortex of rats at different postnatal ages. Within the cortex, only a few labelled cells were observed. These cells were confined to the vicinity of the injection site and their number depended on the animal's age at the time of injection. Labelled cells were absent at postnatal day (PD) 10 but could be detected between PD 14 and PD 18. They then decreased in number over the following period and were not detected in adult animals. Outside the cortex, neurons of the lateral geniculate nucleus (LGN) were not observed to take up and retrogradely transport NGF at any age after birth. In contrast, retrogradely labelled neurons were found in the basal forebrain. Labelled cells were first observed here at PD 14 and then increased in number until reaching the adult pattern. Our results show that intrinsic and extrinsic neurons are labelled following intracortical injections of iodinated NGF. In both neuronal populations, the uptake and transport of NGF is present over a period corresponding to the critical period for visual cortical plasticity. These findings suggest that NGF may play a role, both intra and extracortically, in plasticity phenomena.

Gene expression changes and molecular pathways mediating activity-dependent plasticity in visual cortex

2006 ◽  
Vol 9 (5) ◽  
pp. 660-668 ◽  
Author(s):  
Daniela Tropea ◽  
Gabriel Kreiman ◽  
Alvin Lyckman ◽  
Sayan Mukherjee ◽  
Hongbo Yu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Visual Cortex ◽  
Molecular Pathways ◽  
Dependent Plasticity ◽  
Activity Dependent

scholarly journals Neuromodulatory influence of norepinephrine during developmental experience-dependent plasticity

2016 ◽  
Vol 116 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Randall M. Golovin ◽  
Nicholas J. Ward
Keyword(s):  
Auditory Cortex ◽  
Critical Period ◽  
Cortical Plasticity ◽  
Functional Redundancy ◽  
Neuronal Circuits ◽  
Critical Periods ◽  
Dependent Plasticity ◽  
Phases Of Development ◽  
Developmental Experience ◽  
Insight Into

Critical periods represent phases of development during which neuronal circuits and their responses can be readily shaped by stimuli. Experience-dependent plasticity that occurs within these critical periods can be influenced in many ways; however, Shepard et al. ( J Neurosci 35: 2432–2437, 2015) recently singled out norepinephrine as an essential driver of this plasticity within the auditory cortex. This work provides novel insight into the mechanisms of critical period plasticity and challenges previous conceptions that a functional redundancy exists between noradrenergic and cholinergic influences on cortical plasticity.

scholarly journals Synaptic Mechanisms of Activity-Dependent Remodeling in Visual Cortex during Monocular Deprivation

2009 ◽  
Vol 2 ◽  
pp. JEN.S2559 ◽  
Author(s):  
Cynthia D. Rittenhouse ◽  
Ania K Majewska
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Neuronal Structure ◽  
Cortical Cells ◽  
Dependent Plasticity ◽  
Cortical Synapses ◽  
Activity Dependent ◽  
Synaptic Mechanisms

It has long been appreciated that in the visual cortex, particularly within a postnatal critical period for experience-dependent plasticity, the closure of one eye results in a shift in the responsiveness of cortical cells toward the experienced eye. While the functional aspects of this ocular dominance shift have been studied for many decades, their cortical substrates and synaptic mechanisms remain elusive. Nonetheless, it is becoming increasingly clear that ocular dominance plasticity is a complex phenomenon that appears to have an early and a late component. Early during monocular deprivation, deprived eye cortical synapses depress, while later during the deprivation open eye synapses potentiate. Here we review current literature on the cortical mechanisms of activity-dependent plasticity in the visual system during the critical period. These studies shed light on the role of activity in shaping neuronal structure and function in general and can lead to insights regarding how learning is acquired and maintained at the neuronal level during normal and pathological brain development.

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.

Sign in / Sign up

Export Citation Format

Share Document