Retinal lesions induce fast intrinsic cortical plasticity in adult mouse visual system

Smolders, Katrien; Vreysen, Samme; Laramée, Marie-Eve; Cuyvers, Annemie; Hu, Tjing-Tjing; Brussel, Leen Van; Eysel, Ulf T.; Nys, Julie; Arckens, Lutgarde

doi:10.1111/ejn.13143

Cited by 7 publications

(13 citation statements)

References 92 publications

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“…Dilating only one pupil completely prevents induction of the phenotype in the other retina, thus providing a useful control when simultaneous testing of the two eyes is desirable. Examples include monocular gene therapy 32 , monocular pharmacological treatments followed by morphological and ERG assays 33 , retinal/specific gene expression, studies of the effects of photoreceptor degeneration on cortical plasticity 34 etc.…”

Section: Discussionmentioning

confidence: 99%

Pattern of retinal morphological and functional decay in a light-inducible, rhodopsin mutant mouse

Gargini

Novelli

Piano

et al. 2017

Sci Rep

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Hallmarks of Retinitis Pigmentosa (RP), a family of genetic diseases, are a typical rod-cone-degeneration with initial night blindness and loss of peripheral vision, followed by decreased daylight sight and progressive visual acuity loss up to legal blindness. Great heterogeneity in nature and function of mutated genes, variety of mutations for each of them, variability in phenotypic appearance and transmission modality contribute to make RP a still incurable disease. Translational research relies on appropriate animal models mimicking the genetic and phenotypic diversity of the human pathology. Here, we provide a systematic, morphological and functional analysis of RhoTvrm4/Rho+ rhodopsin mutant mice, originally described in 2010 and portraying several features of common forms of autosomal dominant RP caused by gain-of-function mutations. These mice undergo photoreceptor degeneration only when exposed briefly to strong, white light and allow controlled timing of induction of rod and cone death, which therefore can be elicited in adult animals, as observed in human RP. The option to control severity and retinal extent of the phenotype by regulating intensity and duration of the inducing light opens possibilities to exploit this model for multiple experimental purposes. Altogether, the unique features of this mutant make it an excellent resource for retinal degeneration research.

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Section: Discussionmentioning

confidence: 99%

Pattern of retinal morphological and functional decay in a light-inducible, rhodopsin mutant mouse

Gargini

Novelli

Piano

et al. 2017

Sci Rep

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“…Optical density measurements of the expression of zif268 , a neuronal activity marker (Arckens et al, 2000a,b; Hu et al, 2009; van Brussel et al, 2009; Van Brussel et al, 2011; Nys et al, 2014; Smolders et al, 2015), allowed the generation of visual activity maps for sighted and ME mice after different post mono-enucleation survival times (Figure 4). Over the time course of 7 weeks, the posterior regions of the striate and extrastriate areas recovered readily, except for the posterior monocular zone of V1 and medial extrastriate cortex.…”

Section: Discussionmentioning

confidence: 99%

“…We performed in situ hybridization for zif268 as described before (van Brussel et al, 2009; Van Brussel et al, 2011; Nys et al, 2014; Aerts et al, 2014b; Smolders et al, 2015). A series of coronal sections between Bregma levels −2.0 and −4.4 mm were selected to span the striate and extrastriate areas.…”

Section: Methodsmentioning

confidence: 99%

“…Cresyl violet stainings provide sufficient information to delineate the primary visual cortex (V1), lateral extrastriate cortex (V2L), medio-lateral extrastriate cortex (V2ML) and medio-medial extrastriate cortex (V2MM) based on the cytoarchitecture as described in detail previously (Caviness, 1975; van Brussel et al, 2009; Van Brussel et al, 2011; Nys et al, 2014, 2015; Smolders et al, 2015) and comparisons were made with the stereotaxic mouse brain atlas (Paxinos and Franklin, 2013). The border annotations for each section were superimposed onto the corresponding autoradiographic image with Adobe Photoshop CS6 before being imported in Matlab (Figure 1A) to aid interpretation of areal borders in the created top views.…”

Section: Methodsmentioning

confidence: 99%

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A Tool for Brain-Wide Quantitative Analysis of Molecular Data upon Projection into a Planar View of Choice

et al. 2017

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Several techniques, allowing the reconstruction and visualization of functional, anatomical or molecular information from tissue and organ slices, have been developed over the years. Yet none allow direct comparison without reprocessing the same slices. Alternative methods using publicly available reference maps like the Allen Brain Atlas lack flexibility with respect to age and species. We propose a new approach to reconstruct a segmented region of interest from serial slices by projecting the optical density values representing a given molecular signal to a plane of view of choice, and to generalize the results into a reference map, which is built from the individual maps of all animals under study. Furthermore, to allow quantitative comparison between experimental conditions, a non-parametric pseudo t-test has been implemented. This new mapping tool was applied, optimized and validated making use of an in situ hybridization dataset that represents the spatiotemporal expression changes for the neuronal activity reporter gene zif268, in relation to cortical plasticity induced by monocular enucleation, covering the entire mouse visual cortex. The created top view maps of the mouse brain allow precisely delineating and interpreting 11 extrastriate areas surrounding mouse V1. As such, and because of the opportunity to create a planar projection of choice, these molecular maps can in the future easily be compared with functional or physiological imaging maps created with other techniques such as Ca2+, flavoprotein and optical imaging.

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“…ISH for zif268 -mRNA was performed with a mouse-specific synthetic oligonucleotide probe (Eurogentec, Seraing, Belgium) with sequence 5′-ccgttgctcagcagcatcatctcctccagtttggggtagttgtcc-3′. As described previously [ 51 , 53 , 77 , 88 ], each probe was 3′-end labeled with [ 33 P] dATP using terminal deoxynucleotidyl transferase (Invitrogen, Carlsbad, CA). Unincorporated nucleotides were separated from the labeled probe by means of miniQuick Spin Oligo Columns (Roche Diagnostics, Vilvoorde, Belgium).…”

Section: Methodsmentioning

confidence: 99%

5-HTR2A and 5-HTR3A but not 5-HTR1A antagonism impairs the cross-modal reactivation of deprived visual cortex in adulthood

et al. 2018

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Visual cortical areas show enhanced tactile responses in blind individuals, resulting in improved behavioral performance. Induction of unilateral vision loss in adult mice, by monocular enucleation (ME), is a validated model for such cross-modal brain plasticity. A delayed whisker-driven take-over of the medial monocular zone of the visual cortex is preceded by so-called unimodal plasticity, involving the potentiation of the spared-eye inputs in the binocular cortical territory. Full reactivation of the sensory-deprived contralateral visual cortex is accomplished by 7 weeks post-injury. Serotonin (5-HT) is known to modulate sensory information processing and integration, but its impact on cortical reorganization after sensory loss, remains largely unexplored. To address this issue, we assessed the involvement of 5-HT in ME-induced cross-modal plasticity and the 5-HT receptor (5-HTR) subtype used. We first focused on establishing the impact of ME on the total 5-HT concentration measured in the visual cortex and in the somatosensory barrel field. Next, the changes in expression as a function of post-ME recovery time of the monoamine transporter 2 (vMAT2), which loads 5-HT into presynaptic vesicles, and of the 5-HTR1A and 5-HTR3A were assessed, in order to link these temporal expression profiles to the different types of cortical plasticity induced by ME. In order to accurately pinpoint which 5-HTR exactly mediates ME-induced cross-modal plasticity, we pharmacologically antagonized the 5-HTR1A, 5-HTR2A and 5-HTR3A subtypes. This study reveals brain region-specific alterations in total 5-HT concentration, time-dependent modulations in vMAT2, 5-HTR1A and 5-HTR3A protein expression and 5-HTR antagonist-specific effects on the post-ME plasticity phenomena. Together, our results confirm a role for 5-HTR1A in the early phase of binocular visual cortex plasticity and suggest an involvement of 5-HTR2A and 5-HTR3A but not 5-HTR1A during the late cross-modal recruitment of the medial monocular visual cortex. These insights contribute to the general understanding of 5-HT function in cortical plasticity and may encourage the search for improved rehabilitation strategies to compensate for sensory loss.

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Retinal lesions induce fast intrinsic cortical plasticity in adult mouse visual system

Cited by 7 publications

References 92 publications

Pattern of retinal morphological and functional decay in a light-inducible, rhodopsin mutant mouse

Pattern of retinal morphological and functional decay in a light-inducible, rhodopsin mutant mouse

A Tool for Brain-Wide Quantitative Analysis of Molecular Data upon Projection into a Planar View of Choice

5-HTR2A and 5-HTR3A but not 5-HTR1A antagonism impairs the cross-modal reactivation of deprived visual cortex in adulthood

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