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.2014.05.022

Cited by 35 publications

(56 citation statements)

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“…In this context, it is possible that PirB is involved with the Nogo/NgR system to regulate adult OD plasticity (38), consistent with the observation that PirB binds NogoA (39). However, although we find significant spine density increases in PirB −/− adult visual cortex along with increased spine stability and LTP, in adult NgR −/− somatosensory cortex only spine turnover is enhanced, suggesting lower spine stability than normal; no frank change in synaptic density was observed in somatosensory cortex in these mice (40). Another receptor, DR6, was also recently found to regulate structural plasticity in adult cortex: horizontal axons of L2/3 pyramidal and inhibitory neurons in somatosensory cortex of adult DR6 −/− mice fail to prune following whisker plucking, and bouton density is increased (13).…”

Section: Pirb a Receptor Linking Synaptic Structure And Plasticity Isupporting

confidence: 90%

PirB regulates a structural substrate for cortical plasticity

Djurišić

Vidal

Mann

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Experience-driven circuit changes underlie learning and memory. Monocular deprivation (MD) engages synaptic mechanisms of ocular dominance (OD) plasticity and generates robust increases in dendritic spine density on L5 pyramidal neurons. Here we show that the paired immunoglobulin-like receptor B (PirB) negatively regulates spine density, as well as the threshold for adult OD plasticity. In PirB −/− mice, spine density and stability are significantly greater than WT, associated with higher-frequency miniature synaptic currents, larger long-term potentiation, and deficient long-term depression. Although MD generates the expected increase in spine density in WT, in PirB −/− this increase is occluded. In adult PirB −/− , OD plasticity is larger and more rapid than in WT, consistent with the maintenance of elevated spine density. Thus, PirB normally regulates spine and excitatory synapse density and consequently the threshold for new learning throughout life.visual cortex | adult plasticity |

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Section: Pirb a Receptor Linking Synaptic Structure And Plasticity Isupporting

confidence: 90%

PirB regulates a structural substrate for cortical plasticity

Djurišić

Vidal

Mann

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…16,17 In the adult CNS, the expression of neuronal Nogo-A remains elevated mainly in plastic regions such as in the hippocampus, olfactory bulb or neocortex, and in the dorsal root ganglia. 12 Nogo-A and NgR1 were shown to regulate synaptic plasticity, for example, long-term potentiation in the hippocampus and in the sensory-motor cortex, [18][19][20][21][22] whereas the effects of neuronal Nogo-A after injury are not yet well understood. During development, neuronal Nogo-A influences neuronal migration, 23,24 survival, 25,26 cell spreading and neurite growth.…”

mentioning

confidence: 99%

Cell type-specific Nogo-A gene ablation promotes axonal regeneration in the injured adult optic nerve

et al. 2014

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Nogo-A is a well-known myelin-enriched inhibitory protein for axonal growth and regeneration in the central nervous system (CNS). Besides oligodendrocytes, our previous data revealed that Nogo-A is also expressed in subpopulations of neurons including retinal ganglion cells, in which it can have a positive role in the neuronal growth response after injury, through an unclear mechanism. In the present study, we analyzed the opposite roles of glial versus neuronal Nogo-A in the injured visual system. To this aim, we created oligodendrocyte (Cnp-Cre þ / À xRtn4/Nogo-A flox/flox ) and neuron-specific (Thy1-Cre tg þ xRtn4 flox/flox ) conditional Nogo-A knock-out (KO) mouse lines. Following complete intraorbital optic nerve crush, both spontaneous and inflammation-mediated axonal outgrowth was increased in the optic nerves of the glia-specific Nogo-A KO mice. In contrast, neuron-specific deletion of Nogo-A in a KO mouse line or after acute gene recombination in retinal ganglion cells mediated by adeno-associated virus serotype 2.Cre virus injection in Rtn4 flox/flox animals decreased axon sprouting in the injured optic nerve. These results therefore show that selective ablation of Nogo-A in oligodendrocytes and myelin in the optic nerve is more effective at enhancing regrowth of injured axons than what has previously been observed in conventional, complete Nogo-A KO mice. Our data also suggest that neuronal Nogo-A in retinal ganglion cells could participate in enhancing axonal sprouting, possibly by cis-interaction with Nogo receptors at the cell membrane that may counteract trans-Nogo-A signaling. We propose that inactivating Nogo-A in glia while preserving neuronal Nogo-A expression may be a successful strategy to promote axonal regeneration in the CNS.

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“…In the neocortex, a temporal coincidence exists between myelin formation in layers IV-VI and the maturation-dependent reduction of plasticity, for example, the closure of the critical window for ocular dominance plasticity (McGee et al 2006). Importantly, developmental levels of structural plasticity could be reestablished in full adult life in Nogo or Nogo receptor (NgR1) knockout (KO) mice in the visual and the sensorimotor cortex (McGee et al 2006;Akbik et al 2013). Similar results were obtained by enzymatic removal of CSPGs (Pizzorusso et al 2006).…”

Section: Myelin-associated Growth Inhibitors Restrict Developmental Pmentioning

confidence: 68%

Central Nervous System Regenerative Failure: Role of Oligodendrocytes, Astrocytes, and Microglia

Silver

Schwab

Popovich

2014

Cold Spring Harb Perspect Biol

282

209

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Animal studies are now showing the exciting potential to achieve significant functional recovery following central nervous system (CNS) injury by manipulating both the inefficient intracellular growth machinery in neurons, as well as the extracellular barriers, which further limit their regenerative potential. In this review, we have focused on the three major glial cell types: oligodendrocytes, astrocytes, and microglia/macrophages, in addition to some of their precursors, which form major extrinsic barriers to regrowth in the injured CNS. Although axotomized neurons in the CNS have, at best, a limited capacity to regenerate or sprout, there is accumulating evidence that even in the adult and, especially after boosting their growth motor, neurons possess the capacity for considerable circuit reorganization and even lengthy regeneration when these glial obstacles to neuronal regrowth are modified, eliminated, or overcome.T he failure of injured central nervous system (CNS) axons to regenerate over long distances and reestablish connections interrupted by traumatic lesions has been known for a very long time. As early as 1890, the striking difference between central axons and the often well-regenerating peripheral nerves was experimentally studied; peripheral nerve grafts were implanted into different parts of the brain, retina, and spinal cord. The results showed that denervated peripheral nerves are excellent growth-promoting substrates for regenerating axons, whether of peripheral or central origin. Santiago Ramó n y Cajal summarized these pioneering studies in his seminal book, Regeneration and Degeneration of the Nervous System (1913 in Spanish; 1928 first English edition; Ramó n y Cajal et al. 1991). He concluded that adult central neurons can be induced to grow long axons by attractive and trophic factors originating from peripheral nerves. He also speculated that the absence of regeneration in CNS tissue would be because of a lack of such factors in the adult brain and spinal cord. Modern tracing

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Anatomical Plasticity of Adult Brain Is Titrated by Nogo Receptor 1

Cited by 35 publications

References 0 publications

PirB regulates a structural substrate for cortical plasticity

PirB regulates a structural substrate for cortical plasticity

Cell type-specific Nogo-A gene ablation promotes axonal regeneration in the injured adult optic nerve

Central Nervous System Regenerative Failure: Role of Oligodendrocytes, Astrocytes, and Microglia

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