Anatomical Plasticity of Adult Brain Is Titrated by Nogo Receptor 1

Akbik, Feras; Bhagat, Sarah M.; Patel, Pujan R.; Cafferty, William B. J.; Strittmatter, Stephen M.

doi:10.1016/j.neuron.2012.12.027

Cited by 101 publications

(104 citation statements)

References 45 publications

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“…Similar to preceding publications [11], [20], [30], we observe that ngr1 −/− mice exhibit a mild deficit in performance. Despite this lower overall performance, ngr1 −/− mice improve over subsequent trials similar to WT mice.…”

Section: Discussionsupporting

confidence: 91%

“…3G). A previous study reported that the 14-day stability of spines in ngr1 −/− mice was quadruple that of WT mice [11]. However, we observe that ngr1 −/− mice display basal spine formation, spine retraction, and new spine stability in barrel cortex that are indistinguishable from WT mice.…”

Section: Resultscontrasting

confidence: 63%

“…A preceding study reported that basal dynamics and stability of dendritic spines and axonal boutons were dramatically elevated in ngr1−/− mice [11]. To determine if the better performance on the gap cross performance correlated with greater basal synaptic structural plasticity, we imaged these synaptic structures in WT and ngr1 −/− mice harboring the EGFP-M transgene in layer I of somatosensory (S1) barrel cortex with chronic in vivo two-photon microscopy (Figures 2–4).…”

Section: Resultsmentioning

confidence: 99%

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Nogo Receptor 1 Limits Tactile Task Performance Independent of Basal Anatomical Plasticity

et al. 2014

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The genes that govern how experience refines neural circuitry and alters synaptic structural plasticity are poorly understood. The nogo-66 receptor 1 gene (ngr1) is one candidate that may restrict the rate of learning as well as basal anatomical plasticity in adult cerebral cortex. To investigate if ngr1 limits the rate of learning we tested adult ngr1 null mice on a tactile learning task. Ngr1 mutants display greater overall performance despite a normal rate of improvement on the gap-cross assay, a whisker-dependent learning paradigm. To determine if ngr1 restricts basal anatomical plasticity in the associated sensory cortex, we repeatedly imaged dendritic spines and axonal varicosities of both constitutive and conditional adult ngr1 mutant mice in somatosensory barrel cortex for two weeks through cranial windows with two-photon chronic in vivo imaging. Neither constant nor acute deletion of ngr1 affected turnover or stability of dendritic spines or axonal boutons. The improved performance on the gap-cross task is not attributable to greater motor coordination, as ngr1 mutant mice possess a mild deficit in overall performance and a normal learning rate on the rotarod, a motor task. Mice lacking ngr1 also exhibit normal induction of tone-associated fear conditioning yet accelerated fear extinction and impaired consolidation. Thus, ngr1 alters tactile and motor task performance but does not appear to limit the rate of tactile or motor learning, nor determine the low set point for synaptic turnover in sensory cortex.

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Section: Discussionsupporting

confidence: 91%

Section: Resultscontrasting

confidence: 63%

Section: Resultsmentioning

confidence: 99%

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Nogo Receptor 1 Limits Tactile Task Performance Independent of Basal Anatomical Plasticity

et al. 2014

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“…These inhibitory ligands may function as "molecular brakes" by signaling through NgR1 to limit structural synaptic plasticity that could contribute to improving acuity after LTMD (Morishita and Hensch, 2008;Holtmaat and Svoboda, 2009). Consistent with this hypothesis, suppressing NgR1 expression in primary hippocampal neurons by RNA interference increases the formation of excitatory synapses in vitro (Wills et al, 2012), and NgR1 mutant mice have been reported to display elevated basal turnover of dendritic spines in visual cortex (Akbik et al, 2013). It would be interesting to examine whether the number of excitatory synapses made onto L2/3 PV interneurons is altered by NgR1 deletion or restoration of normal vision following LTMD may differentially affect structural synaptic plasticity in NgR1 mutant mice.…”

Section: Discussionmentioning

confidence: 86%

Plasticity of Binocularity and Visual Acuity Are Differentially Limited by Nogo Receptor

et al. 2014

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The closure of developmental critical periods consolidates neural circuitry but also limits recovery from early abnormal sensory experience. Degrading vision by one eye throughout a critical period both perturbs ocular dominance (OD) in primary visual cortex and impairs visual acuity permanently. Yet understanding how binocularity and visual acuity interrelate has proven elusive. Here we demonstrate the plasticity of binocularity and acuity are separable and differentially regulated by the neuronal nogo receptor 1 (NgR1). Mice lacking NgR1 display developmental OD plasticity as adults and their visual acuity spontaneously improves after prolonged monocular deprivation. Restricting deletion of NgR1 to either cortical interneurons or a subclass of parvalbumin (PV)-positive interneurons alters intralaminar synaptic connectivity in visual cortex and prevents closure of the critical period for OD plasticity. However, loss of NgR1 in PV neurons does not rescue deficits in acuity induced by chronic visual deprivation. Thus, NgR1 functions with PV interneurons to limit plasticity of binocularity, but its expression is required more extensively within brain circuitry to limit improvement of visual acuity following chronic deprivation.

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“…However, spine density is normal in both ngr1 Ϫ/Ϫ mice and transgenic mice overexpressing NgR1 (Lee et al, 2008;Karlén et al, 2009). Likewise, ngr1 Ϫ/Ϫ mice have been reported to display both dramatically elevated spine formation and new spine stability in vivo (Akbik et al, 2013). Yet we have performed similar, in some cases nearly identical, experiments with the same strain of ngr1 Ϫ/Ϫ mice, but we are unable to reproduce these findings.…”

Section: Discussionmentioning

confidence: 99%

Nogo Receptor 1 Confines a Disinhibitory Microcircuit to the Critical Period in Visual Cortex

et al. 2016

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A characteristic of the developing mammalian visual system is a brief interval of plasticity, termed the "critical period," when the circuitry of primary visual cortex is most sensitive to perturbation of visual experience. Depriving one eye of vision (monocular deprivation [MD]) during the critical period alters ocular dominance (OD) by shifting the responsiveness of neurons in visual cortex to favor the nondeprived eye. A disinhibitory microcircuit involving parvalbumin-expressing (PV) interneurons initiates this OD plasticity. The gene encoding the neuronal nogo-66-receptor1(ngr1/rtn4r)isrequiredtoclosethecriticalperiod.Herewecombinedmousegenetics,electrophysiology,andcircuitmapping with laser-scanning photostimulation to investigate whether disinhibition is confined to the critical period by ngr1. We demonstrate that ngr1 mutant mice retain plasticity characteristic of the critical period as adults, and that ngr1 operates within PV interneurons to restrict the loss of intracortical excitatory synaptic input following MD in adult mice, and this disinhibition induces a "lower PV network configuration" in both critical-period wild-type mice and adult ngr1 Ϫ/Ϫ mice. We propose that ngr1 limits disinhibition to close the critical period for OD plasticity and that a decrease in PV expression levels reports the diminished recent cumulative activity of these interneurons.

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Anatomical Plasticity of Adult Brain Is Titrated by Nogo Receptor 1

Cited by 101 publications

References 45 publications

Nogo Receptor 1 Limits Tactile Task Performance Independent of Basal Anatomical Plasticity

Nogo Receptor 1 Limits Tactile Task Performance Independent of Basal Anatomical Plasticity

Plasticity of Binocularity and Visual Acuity Are Differentially Limited by Nogo Receptor

Nogo Receptor 1 Confines a Disinhibitory Microcircuit to the Critical Period in Visual Cortex

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