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• W2064831567 abstract "Normally, the brain can be shaped by sensory experience only during a so-called critical period early in life. Recent research has shed light on the factors determining the end of the critical period, and on how cortical plasticity might be re-established in adulthood. Normally, the brain can be shaped by sensory experience only during a so-called critical period early in life. Recent research has shed light on the factors determining the end of the critical period, and on how cortical plasticity might be re-established in adulthood. And he took the blind man by the hand, and led him out of the village; and when he had spit on his eyes and laid his hands upon him, he asked him, “Do you see anything?” And he looked up and said, “I see men; but they look like trees, walking.” Then he laid his hands upon his eyes; and he looked intently and was restored and saw everything clearly. — Mark 8, 23-25 It is a well-known dogma of neuroscience that the adult mammalian brain has little or no capacity to regenerate or repair after injury. Equally, if adequate stimulation is lacking during a critical or sensitive period in early childhood, certain cortical functions, such as sight or language, will never develop properly later on. Now, several converging lines of research suggest that the ability of the brain to undergo regeneration or plastic changes does not simply fade away as we grow older, but is actively inhibited, and that a number of the factors which prevent regeneration in the adult brain are also involved in the closure of the critical period. The dual role of one of those inhibitors, the myelin-associated protein Nogo-A (Nogo for short), is highlighted in a recent study of experience-dependent plasticity in the mouse visual cortex [1McGee A.W. Yang Y. Fischer Q.S. Daw N.W. Strittmatter S.M. Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor.Science. 2005; 309: 2222-2226Crossref PubMed Scopus (493) Google Scholar]. Nogo-A was first discovered in the myelin sheath of spinal-cord axons, where it is located on the periaxonal side, in close proximity to the axons. It is recognized by the Nogo receptor NgR, which is present on the extracellular side of the neuronal membrane. Intracellular signalling appears to be mediated through the low-affinity neurotrophin receptor p75, with which NgR forms a complex and through which it activates the Rho pathway (Figure 1). The GTPase Rho and its effector, Rho kinase (ROCK) are important regulators of the actin cytoskeleton, and their activation causes growth cone collapse and inhibits axonal growth [2Niederöst B. Oertle T. Fritsche J. McKinney R.A. Bandtlow C.E. Nogo-A and myelin-associated glycoprotein mediate neurite growth inhibition by antagonistic regulation of RhoA and Rac1.J. Neurosci. 2002; 22: 10368-10376Crossref PubMed Google Scholar]. Hence, Nogo is a major contributor to the failure of the spinal cord to recover from injury, despite some initial axonal sprouting [3Schwab M.E. Nogo and axon regeneration.Curr. Opin. Neurobiol. 2004; 14: 118-124Crossref PubMed Scopus (521) Google Scholar]. But what do Nogo and NgR have to do with experience-dependent plasticity of the visual cortex? Quite a lot, according to the latest study from Strittmatter's lab [1McGee A.W. Yang Y. Fischer Q.S. Daw N.W. Strittmatter S.M. Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor.Science. 2005; 309: 2222-2226Crossref PubMed Scopus (493) Google Scholar]. In the past few years, a number of papers have addressed the question: what is critical about the critical period? In particular, what makes the visual cortex more or less insensitive to gross changes in visual experience after a certain age? The standard experimental paradigm of visual cortical plasticity is monocular deprivation, the prevention of vision through one eye by lid suture. During the critical period, this intervention causes profound loss of vision through the affected eye, resulting in a condition known as amblyopia or ‘lazy eye’. Cortical neurons previously responsive to visual stimulation of either eye lose their input from the deprived eye; they shift their so-called ocular dominance towards the open eye. After the critical period monocular deprivation has no such effects. McGee and colleagues [1McGee A.W. Yang Y. Fischer Q.S. Daw N.W. Strittmatter S.M. Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor.Science. 2005; 309: 2222-2226Crossref PubMed Scopus (493) Google Scholar] tested the hypothesis that intracortical myelin, via Nogo/NgR, blocks cortical plasticity by inhibiting neurite outgrowth, similar to the way it blocks axonal regeneration after spinal cord injury. They first characterized the density and laminar distribution of NgR and its ligands in mouse visual cortex. While total levels of myelin as well as of NgR increased only slightly during the critical period, layer 4 (where inputs from the two eyes arrive) showed the greatest increase in myelin. They then assessed the effects of four days of monocular deprivation in normal mice as compared with mutants lacking either Nogo-A [4Kim J.E. Li S. GrandPre T. Qiu D. Strittmatter S.M. Axon regeneration in young adult mice lacking Nogo-A/B.Neuron. 2003; 38: 187-199Abstract Full Text Full Text PDF PubMed Scopus (369) Google Scholar] or NgR [5Kim J.E. Liu B.P. Park J.H. Strittmatter S.M. Nogo-66 receptor prevents raphespinal and rubrospinal axon regeneration and limits functional recovery from spinal cord injury.Neuron. 2004; 44: 439-451Abstract Full Text Full Text PDF PubMed Scopus (298) Google Scholar]. Normally reared mutant mice exhibited normal responses to visual stimulation and a normal ocular dominance profile. When monocularly deprived during the critical period (starting at age 24 days), they showed the same shift in ocular dominance towards the open eye as wild-type mice. Crucially, when monocular deprivation was imposed after the end of the critical period (aged 45 days), as determined in normal mice, the mice lacking Nogo or NgR exhibited an undiminished ocular dominance shift, while the wild-type mice showed no such shift. This result did not simply reflect a delay in the time course of the critical period, as a pronounced ocular dominance shift was seen even when deprivation was imposed in four-month-old mice. The absence of either Nogo or NgR thus prevents the closure of the critical period and preserves plasticity, perhaps indefinitely. McGee and colleagues [1McGee A.W. Yang Y. Fischer Q.S. Daw N.W. Strittmatter S.M. Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor.Science. 2005; 309: 2222-2226Crossref PubMed Scopus (493) Google Scholar] further addressed the question: which signalling pathways might mediate the Nogo/NgR effects on cortical plasticity? We are now beginning to understand that the maturation of inhibitory circuitry in the cortex — where transmission is mediated by γ-amino butyric acid (GABA) — which somewhat lags behind excitatory connections, is crucial in controlling both the opening [6Fagiolini M. Hensch T.K. Inhibitory threshold for critical-period activation in primary visual cortex.Nature. 2000; 404: 183-186Crossref PubMed Scopus (526) Google Scholar] and closure of the critical period. Moreover, towards the end of the critical period, chondroitin sulphate proteoglycans (CSPGs) in the extracellular matrix aggregate and form perineuronal nets, primarily around parvalbumin-positive inhibitory neurons, thus contributing to the blockade of neurite outgrowth [7Bradbury E.J. Moon L.D.F. Popat R.J. King V.R. Bennett G.S. Patel P.N. Fawcett J.W. McMahon S.B. Chondroitinase ABC promotes functional recovery after spinal cord injury.Nature. 2002; 416: 636-640Crossref PubMed Scopus (1900) Google Scholar, 8Silver J. Miller J.H. Regeneration beyond the glial scar.Nat. Rev. Neurosci. 2004; 5: 146-156Crossref PubMed Scopus (2379) Google Scholar] and visual cortical plasticity [9Pizzorusso T. Medini P. Berardi N. Chierzi S. Fawcett J.W. Maffei L. Reactivation of ocular dominance plasticity in the adult visual cortex.Science. 2002; 298: 1248-1251Crossref PubMed Scopus (1251) Google Scholar]. Additionally, the extracellular protease tissue plasminogen activator (tPA) is known to play a role in monocular deprivation effects and their reversal [10Müller C.M. Griesinger C.B. Tissue plasminogen activator mediates reverse occlusion plasticity in visual cortex.Nat. Neurosci. 1998; 1: 47-53Crossref PubMed Scopus (93) Google Scholar], either directly or through activation of plasmin. CSPGs are among the many targets of these enzymes, which appear to be key regulators of dendritic spine motility, critical for synaptic plasticity [11Mataga N. Mizuguchi Y. Hensch T.K. Experience-dependent pruning of dendritic spines in visual cortex by tissue plasminogen activator.Neuron. 2004; 44: 1031-1041Abstract Full Text Full Text PDF PubMed Scopus (286) Google Scholar, 12Oray S. Majewska A. Sur M. Dendritic spine dynamics are regulated by monocular deprivation and extracellular matrix degradation.Neuron. 2004; 44: 1021-1030Abstract Full Text Full Text PDF PubMed Scopus (237) Google Scholar]. Interestingly, the Nogo/NgR-dependent regulation of visual cortical plasticity does not seem to involve a change in GABAergic inhibition or tPA activity, as parvalbumin and tPA immunoreactivity are normal in NgR knock-out mice [1McGee A.W. Yang Y. Fischer Q.S. Daw N.W. Strittmatter S.M. Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor.Science. 2005; 309: 2222-2226Crossref PubMed Scopus (493) Google Scholar]. Therefore, Nogo/NgR must act either independently or further downstream in the signalling cascade. The implications of this work are more far-reaching than just adding to a growing body of evidence of what controls plasticity in the central nervous system. Knowledge of what prevents it in adulthood offers the opportunity to develop therapeutic strategies to overcome this inhibition. These might entail inactivation of Nogo with antibodies or fusion proteins [13Chen M.S. Huber A.B. van der Haar M.E. Frank M. Schnell L. Spillmann A.A. Christ F. Schwab M.E. Nogo-A is a myelin-associated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1.Nature. 2000; 403: 434-439Crossref PubMed Scopus (333) Google Scholar, 14Fournier A.E. Gould G.C. Liu B.P. Strittmatter S.M. Truncated soluble Nogo receptor binds Nogo-66 and blocks inhibition of axon growth by myelin.J. Neurosci. 2002; 22: 8876-8883Crossref PubMed Google Scholar] or blockade of NgR with a peptide derived from the first 40 amino acids of the Nogo-66 binding region of Nogo [15GrandPre T. Li S. Strittmatter S.M. Nogo-66 receptor antagonist peptide promotes axonal regeneration.Nature. 2002; 417: 547-551Crossref PubMed Scopus (665) Google Scholar], or modifications of the extracellular matrix [9Pizzorusso T. Medini P. Berardi N. Chierzi S. Fawcett J.W. Maffei L. Reactivation of ocular dominance plasticity in the adult visual cortex.Science. 2002; 298: 1248-1251Crossref PubMed Scopus (1251) Google Scholar]. Potential applications include not only regeneration of severed nerves but also treatment of, for example, amblyopia. This is still the most widespread developmental disorder of vision, affecting 2%–4% of the population, and in case of persistence into adulthood is a significant risk factor for blindness in the case of an individual losing sight in the other eye. In the UK alone 370 patients suffered vision loss in the non-amblyopic eye during a two-year period, 86 of whom were severely visually impaired or blind [16Rahi J. Logan S. Timms C. Russell-Eggitt I. Taylor D. Risk, causes, and outcomes of visual impairment after loss of vision in the non-amblyopic eye: a population-based study.Lancet. 2002; 360: 597-602Abstract Full Text Full Text PDF PubMed Scopus (196) Google Scholar]. If we were able to re-establish visual cortical plasticity in adulthood, this would provide a chance to restore vision in an amblyopic eye after the end of the critical period. But a question that will need to be addressed beforehand is this: is there a good reason for plasticity to be limited in the mammalian brain, and what will be the price to pay for allowing plasticity in adulthood?" @default.
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• W2064831567 title "Visual Cortex: Overcoming a No-Go for Plasticity" @default.
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