2000
DOI: 10.1002/1097-4695(20001105)45:2<120::aid-neu6>3.0.co;2-6
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Nitric oxide modulates retinal ganglion cell axon arbor remodelingin vivo

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Cited by 41 publications
(19 citation statements)
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“…The literature indicates that SH-SY5Y neurites are primarily axonal (Haque et al, 1999;Encinas et al, 2000), and our own data (data not shown) demonstrating high levels of tau in these cells confirm the results from earlier studies. The current data support previous work demonstrating that axon branching is separable from other aspects of neurite outgrowth (Weeks et al, 1991;Cogen and Cohen-Cory, 2000;Markus et al, 2002). Therefore, we hypothesize that Rit functions in neurons to increase axonal arborization during target innervation and/or synaptic plasticity events.…”
Section: Rit and Neuronal Development/regenerationsupporting
confidence: 91%
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“…The literature indicates that SH-SY5Y neurites are primarily axonal (Haque et al, 1999;Encinas et al, 2000), and our own data (data not shown) demonstrating high levels of tau in these cells confirm the results from earlier studies. The current data support previous work demonstrating that axon branching is separable from other aspects of neurite outgrowth (Weeks et al, 1991;Cogen and Cohen-Cory, 2000;Markus et al, 2002). Therefore, we hypothesize that Rit functions in neurons to increase axonal arborization during target innervation and/or synaptic plasticity events.…”
Section: Rit and Neuronal Development/regenerationsupporting
confidence: 91%
“…For example, Akt (Markus et al, 2002), cAMP (Weeks et al, 1991) and nitric oxide (Cogen and Cohen-Cory, 2000) modulate axon branching, which is differentially affected by trophic factors (Gallo and Letourneau, 1998;Szebenyi et al, 2001) and extracellular matrix molecules (Weeks et al, 1991). We propose that Rit activates a novel pathway to promote neurite outgrowth and branching (Kuo et al, 1996;Morooka and Nishida, 1998;Lehmann et al, 1999;Anneren et al, 2000;Brown et al, 2000;Ghil et al, 2000;Klocker et al, 2000;Burry, 2001).…”
Section: Rit and Extracellular Matrix Interactionsmentioning
confidence: 96%
“…Furthermore, BDNF can be retrogradely transported from RGC axon terminals to the soma/dendrites (23), resulting in an enhanced growth of RGC dendrites (23) and a reduced apoptosis of RGCs (21). However, NO disrupts RGC axon growth in the optic tectum (38) and acts as a retrograde signal to increase neuronal apoptosis (21). Because LTP/LTD may be causally related to the stabilization/elimination of synapse, BDNF-dependent LTP and NO-dependent LTD at retinotectal synapses may contribute to the refinement of the retinotopic map in the optic tectum (4,37,45).…”
Section: Discussionmentioning
confidence: 99%
“…NADPH diaphorase staining to reveal NO synthasepositive cells labeled a population of neurons but not radial glia in the tectum (data not shown; Cogen and Cohen-Cory, 2000). NO synthesis is known to be dependent on calcium entry into neurons via NMDARs, making it a good candidate to mediate neuron-glial signaling (Bredt and Snyder, 1992;Zhuo et al, 1999;Metea and Newman, 2006).…”
Section: Neuronal-activity-dependent Calcium Transients In Radial Gliamentioning
confidence: 97%