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Visual cortex: overcoming a no-go for plasticity

Sengpiel, Frank 2005. Visual cortex: overcoming a no-go for plasticity. Current Biology 15 (24) , R1000-R1002. 10.1016/j.cub.2005.11.050

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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. 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 [1]. 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 [2]. Hence, Nogo is a major contributor to the failure of the spinal cord to recover from injury, despite some initial axonal sprouting [3]. 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 [1].

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Neuroscience and Mental Health Research Institute (NMHRI)
Subjects: Q Science > QP Physiology
Publisher: Elsevier
ISSN: 0960-9822
Last Modified: 02 May 2019 11:45
URI: http://orca.cf.ac.uk/id/eprint/62405

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