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MiR-132, an experience-dependent microRNA, is essential for visual cortex plasticity.

ABSTRACT: Using quantitative analyses, we identified microRNAs (miRNAs) that were abundantly expressed in visual cortex and that responded to dark rearing and/or monocular deprivation. The most substantially altered miRNA, miR-132, was rapidly upregulated after eye opening and was delayed by dark rearing. In vivo inhibition of miR-132 in mice prevented ocular dominance plasticity in identified neurons following monocular deprivation and affected the maturation of dendritic spines, demonstrating its critical role in the plasticity of visual cortex circuits.

SUBMITTER: Mellios N

PROVIDER: S-EPMC3183341 | biostudies-literature | 2011 Sep

REPOSITORIES: biostudies-literature

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miR-132, an experience-dependent microRNA, is essential for visual cortex plasticity.

Mellios Nikolaos N Sugihara Hiroki H Castro Jorge J Banerjee Abhishek A Le Chuong C Kumar Arooshi A Crawford Benjamin B Strathmann Julia J Tropea Daniela D Levine Stuart S SS Edbauer Dieter D Sur Mriganka M

Nature neuroscience 20110904 10

Using quantitative analyses, we identified microRNAs (miRNAs) that were abundantly expressed in visual cortex and that responded to dark rearing and/or monocular deprivation. The most substantially altered miRNA, miR-132, was rapidly upregulated after eye opening and was delayed by dark rearing. In vivo inhibition of miR-132 in mice prevented ocular dominance plasticity in identified neurons following monocular deprivation and affected the maturation of dendritic spines, demonstrating its critic ...[more]

PMID: 21892155

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Experience-dependent expression of miR-132 regulates ocular dominance plasticity.

Project description:miR-132 is a CREB-induced microRNA that is involved in dendritic spine plasticity. We found that visual experience regulated histone post-translational modifications at a CRE locus that is important for miR-212 and miR-132 cluster transcription, and regulated miR-132 expression in the visual cortex of juvenile mice. Monocular deprivation reduced miR-132 expression in the cortex contralateral to the deprived eye. Counteracting this miR-132 reduction with an infusion of chemically modified miR-132 mimic oligonucleotides completely blocked ocular dominance plasticity.

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MiR-29 coordinates age-dependent plasticity brakes in the adult visual cortex

Project description:Visual cortical circuits show profound plasticity during early life and are later stabilized by molecular "brakes" limiting excessive circuit rewiring beyond a critical period. How the appearance of these factors is coordinated during the transition from development to adulthood remains unknown. We analyzed the role of miR-29a, a miRNA targeting factors involved in several important pathways for plasticity such as extracellular matrix and chromatin regulation. We found that visual cortical miR-29a expression in the visual cortex dramatically increases with age, but it is not experience-dependent. Precocious high levels of miR-29a induced by targeted intracortical injections of a miR-29a mimic blocked ocular dominance plasticity and caused an early appearance of perineuronal nets. Conversely, inhibition of miR-29a in adult mice using LNA antagomirs activated ocular dominance plasticity, reduced perineuronal net intensity and number, and changed their chemical composition restoring permissive low chondroitin 4-O-sulfation levels characteristic of juvenile mice. Activated adult plasticity had the typical functional and proteomic signature of juvenile plasticity. Transcriptomic and proteomic studies indicated that miR-29a manipulation regulates the expression of plasticity factors acting at different cellular levels, from chromatin regulation to synaptic organization and extracellular matrix remodeling. Intriguingly, the projection of miR-29a regulated gene dataset onto cell-specific transcriptomes revealed that parvalbumin-positive interneurons and oligodendrocytes were the most affected cells. Overall, miR29a is a master regulator of the age-dependent plasticity brakes promoting stability of visual cortical circuits.

2020-11-04 | PXD016430 | Pride

MiR-29 coordinates age-dependent plasticity brakes in the adult visual cortex

2020-11-04 | PXD016358 | Pride

MiR-29 coordinates age-dependent plasticity brakes in the adult visual cortex.

Project description:Visual cortical circuits show profound plasticity during early life and are later stabilized by molecular "brakes" limiting excessive rewiring beyond a critical period. The mechanisms coordinating the expression of these factors during the transition from development to adulthood remain unknown. We found that miR-29a expression in the visual cortex dramatically increases with age, but it is not experience-dependent. Precocious high levels of miR-29a blocked ocular dominance plasticity and caused an early appearance of perineuronal nets. Conversely, inhibition of miR-29a in adult mice using LNA antagomirs activated ocular dominance plasticity, reduced perineuronal nets, and restored their juvenile chemical composition. Activated adult plasticity had the typical functional and proteomic signature of critical period plasticity. Transcriptomic and proteomic studies indicated that miR-29a manipulation regulates the expression of plasticity brakes in specific cortical circuits. These data indicate that miR-29a is a regulator of the plasticity brakes promoting age-dependent stabilization of visual cortical connections.

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Sex and estrous cycle affect experience-dependent plasticity in mouse primary visual cortex

Project description:Sex hormones can affect cellular physiology and modulate synaptic plasticity, but it is not always clear whether or how sex-dependent differences identified in vitro express themselves as functional dimorphisms in the brain. Historically, most experimental neuroscience has been conducted using only male animals and the literature is largely mute about whether including female mice in will introduce variability due to inherent sex differences or endogenous estrous cycles. Though this is beginning to change following an NIH directive that sex should be included as a factor in vertebrate research, the lack of information raises practical issues around how to design experimental controls and apply existing knowledge to more heterogeneous populations. Various lines of research suggest that visual processing can be affected by sex and estrous cycle stage. For these reasons, we performed a series of in vivo electrophysiological experiments to characterize baseline visual function and experience-dependent plasticity in the primary visual cortex (V1) of male and female mice. We find that sex and estrous stage have no statistically significant effect on baseline acuity measurements, but that both sex and estrous stage have can modulate two mechanistically distinct forms of experience dependent cortical plasticity. We also demonstrate that resulting variability can be largely controlled with appropriate normalizations. These findings suggest that V1 plasticity can be used for mechanistic studies focusing on how sex hormones effect experience dependent plasticity in the mammalian cortex.

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Inhibition of Cdk5 in PV Neurons Reactivates Experience-Dependent Plasticity in Adult Visual Cortex.

Project description:Cyclin-dependent kinase 5 (Cdk5) has been shown to play a critical role in brain development, learning, memory and neural processing in general. Cdk5 is widely distributed in many neuron types in the central nervous system, while its cell-specific role is largely unknown. Our previous study showed that Cdk5 inhibition restored ocular dominance (OD) plasticity in adulthood. In this study, we specifically knocked down Cdk5 in different types of neurons in the visual cortex and examined OD plasticity by optical imaging of intrinsic signals. Downregulation of Cdk5 in parvalbumin-expressing (PV) inhibitory neurons, but not other neurons, reactivated adult mouse visual cortical plasticity. Cdk5 knockdown in PV neurons reduced the evoked firing rate, which was accompanied by an increment in the threshold current for the generation of a single action potential (AP) and hyperpolarization of the resting membrane potential. Moreover, chemogenetic activation of PV neurons in the visual cortex can attenuate the restoration of OD plasticity by Cdk5 inhibition. Taken together, our results suggest that Cdk5 in PV interneurons may play a role in modulating the excitation and inhibition balance to control the plasticity of the visual cortex.

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MiR-29 coordinates age-dependent plasticity brakes in the adult visual cortex

Project description:Visual cortical circuits show profound plasticity during early life and are later stabilized by molecular "brakes" limiting excessive rewiring beyond a critical period. The mechanisms coordinating the expression of these factors during the transition from development to adulthood remain unknown. We found that miR-29a expression in the visual cortex dramatically increases with age, but it is not experience-dependent. Precocious high levels of miR-29a blocked ocular dominance plasticity and caused an early appearance of perineuronal nets. Conversely, inhibition of miR-29a in adult mice using LNA antagomirs activated ocular dominance plasticity, reduced perineuronal nets and restored their juvenile chemical composition. Activated adult plasticity had the typical functional and proteomic signature of critical period plasticity. Transcriptomic and proteomic studies indicated that miR-29a manipulation regulates the expression of plasticity brakes mainly affecting parvalbumin-positive interneurons. These data indicate that miR29a is a master regulator of the plasticity brakes promoting age-dependent stabilization of visual cortical circuits.

2020-11-03 | GSE141734 | GEO

A Primer on Constructing Plasticity Phenotypes to Classify Experience-Dependent Development of the Visual Cortex.

Project description:Many neural mechanisms regulate experience-dependent plasticity in the visual cortex (V1), and new techniques for quantifying large numbers of proteins or genes are transforming how plasticity is studied into the era of big data. With those large data sets comes the challenge of extracting biologically meaningful results about visual plasticity from data-driven analytical methods designed for high-dimensional data. In other areas of neuroscience, high-information content methodologies are revealing more subtle aspects of neural development and individual variations that give rise to a richer picture of brain disorders. We have developed an approach for studying V1 plasticity that takes advantage of the known functions of many synaptic proteins for regulating visual plasticity. We use that knowledge to rebrand protein measurements into plasticity features and combine those into a plasticity phenotype. Here, we provide a primer for analyzing experience-dependent plasticity in V1 using example R code to identify high-dimensional changes in a group of proteins. We describe using PCA to classify high-dimensional plasticity features and use them to construct a plasticity phenotype. In the examples, we show how to use this analytical framework to study and compare experience-dependent development and plasticity of V1 and apply the plasticity phenotype to translational research questions. We include an R package "PlasticityPhenotypes" that aggregates the coding packages and custom code written in RStudio to construct and analyze plasticity phenotypes.

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Rapid experience-dependent plasticity of synapse function and structure in ferret visual cortex in vivo.

Project description:The rules by which visual experience influences neuronal responses and structure in the developing brain are not well understood. To elucidate the relationship between rapid functional changes and dendritic spine remodeling in vivo, we carried out chronic imaging experiments that tracked visual responses and dendritic spines in the ferret visual cortex following brief periods of monocular deprivation. Functional changes, which were largely driven by loss of deprived eye responses, were tightly regulated with structural changes at the level of dendritic spines, and occurred very rapidly (on a timescale of hours). The magnitude of functional changes was correlated with the magnitude of structural changes across the cortex, and both these features reversed when the deprived eye was reopened. A global rule governed how the responses to the two eyes or changes in spines were altered by monocular deprivation: the changes occurred irrespective of regional ocular dominance preference and were independently mediated by each eye, and the loss or gain of responses/spines occurred as a constant proportion of predeprivation drive by the deprived or nondeprived eye, respectively.

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Tumor necrosis factor-alpha mediates one component of competitive, experience-dependent plasticity in developing visual cortex.

Project description:Rapid, experience-dependent plasticity in developing visual cortex is thought to be competitive. After monocular visual deprivation, the reduction in response of binocular neurons to one eye is matched by a corresponding increase to the other. Chronic optical imaging in mice deficient in TNFalpha reveals the normal initial loss of deprived-eye responses, but the subsequent increase in response to the open eye is absent. This mutation also blocks homeostatic synaptic scaling of mEPSCs in visual cortex in vitro, without affecting LTP. In monocular cortex, thought not to be subject to competition, responses in TNFalpha mutants are as reduced as in the binocular zone. Pharmacological inhibition of endogenous TNFalpha in wild-type mice phenocopies the knockout. These findings suggest that experience-dependent competition in developing visual cortex is the outcome of two distinct, noncompetitive processes, a loss of deprived-eye responses followed by an apparently homeostatic increase in responses dependent on TNFalpha signaling.

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