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1 fects from inhibition of macrophage-mediated axonal retraction.
2 and microglia required activation to induce axonal retraction.
3 phages and dystrophic axons led to extensive axonal retraction.
4 hat alterations in the cytoskeleton underlie axonal retraction.
5 tiple concentrations significantly inhibited axonal retraction.
6 ar mechanisms underlying macrophage-mediated axonal retraction and demonstrate modifications that can
7 d microglia activation, neuronal cell death, axonal retraction, and development of neuropathic pain.
8 te a direct role of activated macrophages in axonal retraction by physical cell-cell interactions wit
9 bition of MMP-9 prevented macrophage-induced axonal retraction despite significant physical interacti
10 tic macrophages coincides with long-distance axonal retraction from the initial site of injury, a del
11 hages resulted in a significant reduction in axonal retraction; however, we saw no evidence of regene
14 substrate also prevented macrophage-induced axonal retraction in the presence of extensive macrophag
15 cation likewise prevented macrophage-induced axonal retraction in vitro and in vivo following spinal
16 posed an alternative hypothesis, namely that axonal retraction involves a backward retreat of cytoske
19 bundant structural plasticity in the form of axonal retraction, neurite extension, and formation of p
20 te dramatic structural plasticity, including axonal retraction, neurite extension, and the developmen
23 receptors where their loss leads to aberrant axonal retraction, the extension of postsynaptic dendrit
24 t not nicardipine, significantly blocked rod axonal retraction when applied up to 6 hours after detac
25 ment produced rapid growth cone collapse and axonal retraction which persisted while MST was present.
26 tudy, we examined the role of macrophages in axonal retraction within the dorsal columns after spinal
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