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1 M may also be required for adult cholinergic axonal sprouting.
2 catecholamines) and initiating compensatory axonal sprouting.
3 p1 in GnRH neurons counteract Sema3A-induced axonal sprouting.
4 l protein that mediates myelin inhibition of axonal sprouting.
5 n the CNS may stabilize the node and prevent axonal sprouting.
6 ing GAP-43 or L1 showed minor enhancement of axonal sprouting.
7 ized aspiration lesions, which do not induce axonal sprouting.
8 t nonhuman primates retains the capacity for axonal sprouting.
9 onous neuronal activity after TCL as well as axonal sprouting.
10 he exception of NGF/Adts, failed to increase axonal sprouting.
13 to prevent neuronal degeneration, stimulate axonal sprouting and ameliorate behavioral deficits in v
14 ing both GAP-43 and L1 showed more extensive axonal sprouting and axonal growth into the proximal por
15 le (NCAM) expression in motor neurons during axonal sprouting and compensatory reinnervation was expl
16 ther actions, however, such as prevention of axonal sprouting and effects on G-protein-coupled recept
17 nction studies, we found that GDF10 produced axonal sprouting and enhanced functional recovery after
18 uromuscular junction denervation by inducing axonal sprouting and enhancing motor neuron viability.
19 ytoplasmic SRF (SRF-DeltaNLS-GFP) stimulated axonal sprouting and facial nerve regeneration in vivo.
20 ved signal mediated by prostacyclin triggers axonal sprouting and functional recovery in a mouse mode
26 expression of GAP43 (P < 0.01), a marker of axonal sprouting and plasticity, in the peri-infarct cor
29 ng nervous system development and facilitate axonal sprouting and regeneration after injury in the ad
30 LRP1 agonists significantly enhance sensory axonal sprouting and regeneration after spinal cord inju
32 ce that ciliary neurotrophic factor promotes axonal sprouting and regeneration in the periphery raise
33 e that the transplantation of BMSCs enhances axonal sprouting and rewiring into the denervated spinal
34 t 5 and 9 d postlesion, during the period of axonal sprouting and synaptogenesis, there was an increa
36 et tissues stimulate sympathetic and sensory axonal sprouting and that an absence of p75NTR by sensor
37 ogo-NogoReceptor (NgR) pathway might enhance axonal sprouting and thereby recovery after focal brain
38 y of spared Nf1-/- DRG neurons for increased axonal sprouting, and by non-cell-autonomous contributio
39 ental switch in mTOR dependency for inducing axonal sprouting, and indicate that PTEN deletion in adu
42 nt of endogenous neurogenesis, angiogenesis, axonal sprouting, and synaptogenesis in the ischaemic br
43 rons, Schwann cell hyperplasia, and aberrant axonal sprouting around the medulla were observed in NGF
44 in the disease, associated with distal motor axonal sprouting as part of the reinnervation response t
45 ancement of the MDM2/p53-IGF1R axis enhances axonal sprouting as well as functional recovery after sp
47 ratum (s.) oriens of the hippocampus exhibit axonal sprouting beyond their normal territory and inner
48 n on AD-related synaptotoxicity and aberrant axonal sprouting by ablating or overexpressing Fyn in hu
49 licated NGF in the regulation of cholinergic axonal sprouting by intact neurons projecting to the hip
50 se results confirm that post-lesion reactive axonal sprouting can be delayed in the central nervous s
51 he ability to respond to growth factors with axonal sprouting, cell hypertrophy, and activation of fu
53 de; with the transcallosal and corticospinal axonal sprouting correlating with functional recovery.
55 ntage of marked differences in the degree of axonal sprouting from contralateral homotypic cortex aft
59 r these proteins in epigenetic regulation of axonal sprouting, growth factor-dependent survival of ne
60 The results showed that estrogen induces axonal sprouting in a brainstem-spinal pathway in the ad
63 expression is increased in association with axonal sprouting in deafferented adult rat hippocampus.
64 ulated during the ovarian cycle and promotes axonal sprouting in hypothalamic neurons secreting gonad
65 ral stem cell development and is a marker of axonal sprouting in mid stages of embryonic development.
66 Stroke induces a unique microenvironment for axonal sprouting in periinfarct cortex, in which growth-
67 t contralateral cortical neurons may undergo axonal sprouting in the denervated striatum following a
79 Knowing the circuit-level determinants of axonal sprouting is important for repairing motor circui
80 emaining viable motor neurons; however, this axonal sprouting is insufficient to compensate for motor
83 connections in areas denervated by a lesion (axonal sprouting) is more widespread than previously tho
84 critical for both proper axonal function and axonal sprouting, is inhibited by stroke and that this i
85 he results suggest that M1 injury results in axonal sprouting near the ischemic injury and the establ
87 l period of neural development that includes axonal sprouting, neurogenesis, and surges of select neu
89 exuberant neurite outgrowth and hippocampal axonal sprouting observed in knock-in mice expressing FA
90 ged in the denervated striatum suggests that axonal sprouting occurred in response to the lesion.
92 reviously demonstrated an unexpected, robust axonal sprouting of contralateral corticostriatal neuron
95 tion (ECS) has been shown recently to induce axonal sprouting of granule cells in the rodent hippocam
97 or all of the cortical hand map; 2) central axonal sprouting of spared primary afferents into the do
98 perilesional tissue, erythropoietin enhanced axonal sprouting of the contralesional, but not ipsilesi
99 ecovery, perilesional tissue remodelling and axonal sprouting of the corticorubral and corticobulbar
101 001), axonal branching (P < 0.001), terminal axonal sprouting (P < 0.001)] were all present to an inc
102 s (TCL) of sensorimotor cortex, which induce axonal sprouting, produced two sequential patterns of lo
104 As part of the disease process, an aberrant axonal sprouting response is known to occur near Abeta d
106 d protein 43 (GAP-43), a molecular marker of axonal sprouting, showed a selective increase in GAP-43
107 n post-stroke angiogenesis, neurogenesis and axonal sprouting suggests a continuum of vascular and ne
109 ing spinal trauma, the limited physiological axonal sprouting that contributes to partial recovery of
110 ynaptic-cellular alterations (e.g., reactive axonal sprouting) that lead to dentate hyperexcitability
112 e added TrkB receptor ligands did not induce axonal sprouting to account for increased inhibitory syn
116 perpetual axonal atrophy, degeneration, and axonal sprouting was observed over time, with increasing
118 s of lesions and in the blockade experiments axonal sprouting was strongly correlated with synchronou
119 n rat cerebellar slice cultures by promoting axonal sprouting with formation of vesicle-filled bouton
120 sters that appears to be caused by excessive axonal sprouting with the formation of new, smaller acet
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