Gap‐43 immunoreactivity and axon regeneration in retinal ganglion cells of the rat

Schaden, Herbert; Stuermer, Claudia A. O.; Bähr, Mathias

doi:10.1002/neu.480251209

Cited by 159 publications

(104 citation statements)

References 31 publications

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“…7a and 7a8) and, as expected from earlier results (Doster et al, 1991;Schaden et al, 1994), anti-GAP-43 immunopositive (Figs. 7b and 7b8).…”

Section: L1 Sc-1 and Tag-1 During Rgc Axon Regeneration Following Ssupporting

confidence: 89%

“…5). That a substantial proportion of surviving RGCs produce and transport GAP-43 into their axons was demonstrated earlier (Doster et al, 1991;Schaden et al, 1994) and was confirmed here.…”

Section: L1 Sc-1 and Tag-1 After Optic Nerve Lesionsupporting

confidence: 84%

“…3f ), which in relation to the L1 mRNA-producing RGCs (in normal rats) were 2% at 2 days, 32% at 5 days, 10% at 7 days, 5% at 14 days, 1% at 21 days, and 0 at 28 days after ONL (Fig. 4a) and were thus similar to counts of GAP-43 protein-producing RGCs (Schaden et al, 1994).…”

Section: L1 Sc-1 and Tag-1 After Optic Nerve Lesionsupporting

confidence: 69%

“…Thus, RGCs that regenerate axons synthesize L1, but fail to upregulate SC-1 and TAG-1. Together with L1, these RGCs produce GAP-43, which is upregulated in a proportion of RGCs upon axotomy (Doster et al, 1991;Schaden et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

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Axon-Regenerating Retinal Ganglion Cells in Adult Rats Synthesize the Cell Adhesion Molecule L1 but Not TAG-1 or SC-1

Jung

Petrausch

Stuermer

1997

Molecular and Cellular Neuroscience

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Retinal ganglion cells (RGCs) in rats regenerate axons in the presence of a PNS nerve graft. To determine if axonregenerating RGCs synthesize cell adhesion/recognition molecules which they possessed during development, retinae were subjected to in situ hybridization with antisense cRNA probes of L1, TAG-1, and SC-1 (and GAP-43 for comparison). L1 and TAG-1 (and GAP-43) proteins on axons were detected with antibodies. L1, TAG-1, and SC-1 (and Gap-43) mRNAs and L1 and TAG-1 (and Gap-43) proteins were expressed by RGCs in embryonic, postnatal, and adult rats. After optic nerve lesion (ONL), the surviving RGCs between 2 and 28 days after ONL continue to express L1. TAG-1 and SC-1 expression, however, is lost. In grafted rats, axon-regenerating RGCs express L1 (together with GAP-43) but neither TAG-1 nor SC-1. Thus, axonal regeneration in grafted rats occurs in the presence of L1 (and GAP-43) but in the absence of TAG-1 and SC-1.

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“…7a and 7a8) and, as expected from earlier results (Doster et al, 1991;Schaden et al, 1994), anti-GAP-43 immunopositive (Figs. 7b and 7b8).…”

Section: L1 Sc-1 and Tag-1 During Rgc Axon Regeneration Following Ssupporting

confidence: 89%

“…5). That a substantial proportion of surviving RGCs produce and transport GAP-43 into their axons was demonstrated earlier (Doster et al, 1991;Schaden et al, 1994) and was confirmed here.…”

Section: L1 Sc-1 and Tag-1 After Optic Nerve Lesionsupporting

confidence: 84%

Section: L1 Sc-1 and Tag-1 After Optic Nerve Lesionsupporting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Axon-Regenerating Retinal Ganglion Cells in Adult Rats Synthesize the Cell Adhesion Molecule L1 but Not TAG-1 or SC-1

Jung

Petrausch

Stuermer

1997

Molecular and Cellular Neuroscience

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“…Adult neuronal populations upregulate regenerationassociated genes (RAGs) after axotomy (Tetzlaff et al, 1991;Schaden et al, 1994;Bonilla et al, 2002;Tanabe et al, 2003;Fischer et al, 2004), and axonal sprouting following CNS injury, including TBI, may be accompanied by reinduction of genes ordinarily associated with developmental axonal growth (Emery et al, 2000;Abankwa et al, 2002;Emery et al, 2003;Mason et al, 2003). Over-expression of SPRRR1A can promote axonal outgrowth in vitro (Bonilla et al, 2002), and following FP brain injury, we observed an increased expression of SPRR1A(+)/NeuN (+) neurons in injured cortex and, to lesser extent, CA3 of the hippocampus although frequent SPRR1A (+)/MAP-2 (−) cells were also evident.…”

Section: Discussionmentioning

confidence: 99%

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Marklund

Fulp

Shimizu

et al. 2006

Experimental Neurology

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Axons show a poor regenerative capacity following traumatic central nervous system (CNS) injury, partly due to the expression of inhibitors of axonal outgrowth, of which Nogo-A is considered the most important. We evaluated the acute expression of Nogo-A, the Nogo-66 receptor (NgR) and the novel small proline-rich repeat protein 1A (SPRR1A, previously undetected in brain), following experimental lateral fluid percussion (FP) brain injury in rats. Immunofluorescence with antibodies against Nogo-A, NgR and SPRR1A was combined with antibodies against the neuronal markers NeuN and microtubule-associated protein (MAP)-2 and the oligodendrocyte marker RIP, while Western blot analysis was performed for Nogo-A and NgR. Brain injury produced a significant increase in Nogo-A expression in injured cortex, ipsilateral external capsule and reticular thalamus from days 1-7 post-injury (P < 0.05) compared to controls. Increased expression of Nogo-A was observed in both RIP-and NeuN positive (+) cells in the ipsilateral cortex, in NeuN (+) cells in the CA3 region of the hippocampus and reticular thalamus and in RIP (+) cells in white matter tracts. Alterations in NgR expression were not observed following traumatic brain injury (TBI). Brain injury increased the extent of SPRR1A expression in the ipsilateral cortex and the CA3 at all post-injury time-points in NeuN (+) cells. The marked increases in Nogo-A and SPRR1A in several important brain regions suggest that although inhibitors of axonal growth may be upregulated, the injured brain is also capable of expressing proteins promoting axonal outgrowth following TBI. KeywordsNogo-A; Nogo-66 receptor; Small proline-rich repeat protein 1A (SPRR1A); Traumatic brain injury; Oligodendrocytes

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Plasticity of the auditory brainstem: Effects of cochlear ablation on GAP-43 immunoreactivity in the rat

1997

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In the adult brain, expression of the growth associated protein GAP-43 may serve as an indicator of synaptic remodeling. We have studied localization and time course of the re-expression of GAP-43 following deafening through cochlear ablation. As a consequence of unilateral cochlear lesioning, a substantial increase in the expression of GAP-43 was observed in the neuropil of all subnuclei of the ipsilateral cochlear nuclear complex. This expression of GAP-43 occurred in well-defined fibers and boutons. In the ventral cochlear nuclei, boutons immunoreactive for GAP-43 were often localized on cell bodies. However, they were found only on selected subpopulations of cochlear nucleus neurons, i.e., on cell bodies containing glutamate or calretinin immunoreactivity, but apparently not on GABAergic neurons. Olivocochlear neurons must have been axotomized by the operation. Following cochlear ablation, a dramatic re-expression of GAP-43 occurred in cell bodies of the ipsilateral lateral superior olive but not in the ventral nucleus of the trapezoid body. Position and number of these cells suggested that most, if not all, of them serve the lateral olivocochlear bundle. However, although axon collaterals are given off by certain types of olivocochlear neurons, a direct involvement of the immunoreactive cell bodies in the emergence of GAP-43 in the cochlear nucleus is not obvious. A transient rise of GAP-43 immunoreactivity that could not be attributed to axotomized neurons was observed in the contralateral dorsal cochlear nucleus and in the ipsilateral inferior colliculus. Given the functional significance attributed to GAP-43, we conclude that the sudden loss of spiral ganglion cells leads to a reactive synaptogenesis in complex patterns across several auditory brainstem nuclei.

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Gap‐43 immunoreactivity and axon regeneration in retinal ganglion cells of the rat

Cited by 159 publications

References 31 publications

Axon-Regenerating Retinal Ganglion Cells in Adult Rats Synthesize the Cell Adhesion Molecule L1 but Not TAG-1 or SC-1

Axon-Regenerating Retinal Ganglion Cells in Adult Rats Synthesize the Cell Adhesion Molecule L1 but Not TAG-1 or SC-1

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Plasticity of the auditory brainstem: Effects of cochlear ablation on GAP-43 immunoreactivity in the rat

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