Poststroke Axonal Sprouting: Axonal sprouting is a process by which a fully differentiated neuron engages a neuronal growth program, elaborate a growth cone, extend an axon or an axon collateral, and form new connections. Examples include the significant axonal sprouting induced by peripheral nerve injury in the sensory cortex of nonhuman primates. In addition, lesions in the retina induce sprouting in the cortical neurons that border the deafferented area. Cerebellar lesions induce the primary sensory cortex to sprout into the motor cortex. Likewise, stroke induces axonal sprouting in periinfarct cortex and connected cortical areas. In nonhuman primates, stroke caused sprouts to extend from the premotor cortex to the primary sensory cortex over distances of up to 1 cm. It takes about twenty eight days after stroke for axonal sprouting to form patterns of anatomical connections that can be detected anatomically. Both GAP 43 (growth cone growth-promoting phosphoprotein) and synaptophysin (a marker for synaptogenesis) can be detected in the periinfarct zone after stroke.
While traumatic brain injury and spinal cord injury do not produce substantial axonal sprouting, stroke provides an environment that is more permissive for axonal sprouting where growth-promoting molecules are substantially produced. Surrounding the infarct where there is an area of apoptotic cell death, stroke forms a glial scar that extends several hundred micrometers into the periinfarct cortex in the rat. Within the glial scar several growth-inhibitory molecules are produced, including chondroitin sulfate proteoglycans (aggrecan, phosphocan, versican, and neurocan), myelin-associated glycoprotein, and semaphorin IIIa ligand and its receptor neurophilin 1. Fortunately, the brain expresses growth-promoting molecules inside the glial scar including CAP23, GAP43, MARCKS, and small proline repeat rich protein 1 (SPRR1). Furthermore, the glial scar is surrounded by a growth-permissive zone in which the growth-promoting molecules are expressed and growth-inhibitory molecules are reduced. This growth-permissive zone corresponds to the zone of poststroke axonal sprouting. The immediate two to three weeks poststroke is the window for axonal sprouting. During this period neuronal growth-promoting genes are induced, growth-inhibitory proteins are removed, and many growth inhibitory genes are not yet induced.
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