Elevated expression of B‐50 (GAP‐43)‐mRNA in a subpopulation of olfactory bulb mitral cells following axotomy

Verhaagen, Joost; Zhang, Yumao; Hamers, Frank P.T.; Gispen, W.H.

doi:10.1002/jnr.490350206

Cited by 26 publications

(9 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We used GAP43 expression [22] and DAPI staining as controls for our initial experiments. We found GAP43 to be evenly distributed throughout the mitral and EPL layers (Fig.…”

Section: Resultsmentioning

confidence: 99%

Novel subdomains of the mouse olfactory bulb defined by molecular heterogeneity in the nascent external plexiform and glomerular layers

et al. 2007

View full text Add to dashboard Cite

Background: In the mouse olfactory system, the role of the olfactory bulb in guiding olfactory sensory neuron (OSN) axons to their targets is poorly understood. What cell types within the bulb are necessary for targeting is unknown. What genes are important for this process is also unknown. Although projection neurons are not required, other cell-types within the external plexiform and glomerular layers also form synapses with OSNs. We hypothesized that these cells are important for targeting, and express spatially differentially expressed guidance cues that act to guide OSN axons within the bulb.

show abstract

“…We used GAP43 expression [22] and DAPI staining as controls for our initial experiments. We found GAP43 to be evenly distributed throughout the mitral and EPL layers (Fig.…”

Section: Resultsmentioning

confidence: 99%

Novel subdomains of the mouse olfactory bulb defined by molecular heterogeneity in the nascent external plexiform and glomerular layers

et al. 2007

View full text Add to dashboard Cite

show abstract

“…B-50/ GAP-43 has been related to terminal axon arbor remodeling (Caroni and Grandes, 1990;Mehta et al, 1993;Verzé et al, 1996). In addition, several adult neuron populations upregulate this protein after axotomy (Skene, 1989(Skene, , 1992Doster et al, 1991;Tetzlaff et al, 1991Tetzlaff et al, , 1994Verhaagen et al, 1993;Schaden et al, 1994), and this expression can be enhanced by growth-promoting environmental cues (Hüll and Bähr, 1994;Robinson, 1994;Vaudano et al, 1995;Chong et al, 1996). Thus, although the precise role of B-50/GAP-43 in axon growth is still debated, its expression has been strictly associated with the plastic and regenerative potential of adult neurons.…”

Section: Abstract: Transgenic Mice; Axon Growth-associated Genes; L7mentioning

confidence: 99%

Targeted Overexpression of the Neurite Growth-Associated Protein B-50/GAP-43 in Cerebellar Purkinje Cells Induces Sprouting after Axotomy But Not Axon Regeneration into Growth-Permissive Transplants

et al. 1997

View full text Add to dashboard Cite

B-50/GAP-43 is a nervous tissue-specific protein, the expression of which is associated with axon growth and regeneration. Its overexpression in transgenic mice produces spontaneous axonal sprouting and enhances induced remodeling in several neuron populations (Aigner et al., 1995;Holtmaat et al., 1995). We examined the capacity of this protein to increase the regenerative potential of injured adult central axons, by inducing targeted B-50/GAP-43 overexpression in Purkinje cells, which normally show poor regenerative capabilities. Thus, transgenic mice were produced in which B-50/GAP-43 overexpression was driven by the Purkinje cell-specific L7 promoter. Uninjured transgenic Purkinje cells displayed normal morphology, indicating that transgene expression does not modify the normal phenotype of these neurons. By contrast, after axotomy numerous transgenic Purkinje cells exhibited profuse sprouting along the axon and at its severed end. Nevertheless, despite these growth phenomena, which never occurred in wild-type mice, the severed transgenic axons were not able to regenerate, either spontaneously or into embryonic neural or Schwann cell grafts placed into the lesion site. Finally, although only a moderate Purkinje cell loss occurred in wild-type cerebella after axotomy, a considerable number of injured transgenic neurons degenerated, but they could be partially rescued by the different transplants placed into the lesion site. Thus, B-50/GAP-43 overexpression substantially modifies Purkinje cell response to axotomy, by inducing growth processes and decreasing their resistance to injury. However, the presence of this protein is not sufficient to enable these neurons to accomplish a full program of axon regeneration.

show abstract

“…However, the cellular origin of GAP-43 in VCN remained elusive. Possible candidates are olivocochlear neurons, which are axotomized after cochlear lesion, because axotomized neurons may induce GAP-43 synthesis (Woolf et al, 1990;Verhaagen et al, 1993;Palacios et al, 1994;Schaden et al, 1994;Liabotis and Schreyer, 1995;Elliott et al, 1997).…”

mentioning

confidence: 99%

Superior olivary contributions to auditory system plasticity: Medial but not lateral olivocochlear neurons are the source of cochleotomy‐induced GAP‐43 expression in the ventral cochlear nucleus

Kraus

Illing

2004

J of Comparative Neurology

View full text Add to dashboard Cite

A unilateral cochlear lesion induces expression of the growth and plasticity-associated protein 43 (GAP-43) in fibers and their varicosities on specific types of postsynaptic profiles in the ventral cochlear nucleus (VCN), suggesting the induction of synaptic remodeling. One candidate population from which GAP-43 might emerge was neurons of the lateral olivocochlear (LOC) system residing in the lateral superior olive (LSO). Upon cochleotomy, these neurons express GAP-43 mRNA and GAP-43 protein. However, retrograde axonal tracing with Fast Blue or biotinylated dextran amine from VCN revealed that the number of 6.8 +/- 1.3 neurons in the whole ipsilateral LSO labeled in normal adult rats was distinctly small and did not rise after cochleotomy. Concluding that LOC neurons cannot be the source of GAP-43 in the VCN, we reinvestigated the pattern of GAP-43 in situ hybridization and found that, after cochleotomy, shell neurons in the regions surrounding the LSO and medial olivocochlear (MOC) neurons in the ventral nucleus of the trapezoid body up-regulated GAP-43 mRNA. We then lesioned these regions by means of stereotaxic injections of kainic acid. Destruction of shell neurons preceding an ipsilateral cochleotomy did not change the emergence of GAP-43 immunoreactivity in the VCN. However, if the contralateral MOC system was lesioned, the rise of GAP-43 immunoreactivity in VCN on the side of the cochleotomy was significantly reduced. We conclude that, after cochlear dysfunction, MOC neurons are the major (if not exclusive) source of synaptic reorganization in the VCN that could possibly entail compensatory activation of the affected ascending auditory pathway.

show abstract

Elevated expression of B‐50 (GAP‐43)‐mRNA in a subpopulation of olfactory bulb mitral cells following axotomy

Cited by 26 publications

References 23 publications

Novel subdomains of the mouse olfactory bulb defined by molecular heterogeneity in the nascent external plexiform and glomerular layers

Novel subdomains of the mouse olfactory bulb defined by molecular heterogeneity in the nascent external plexiform and glomerular layers

Targeted Overexpression of the Neurite Growth-Associated Protein B-50/GAP-43 in Cerebellar Purkinje Cells Induces Sprouting after Axotomy But Not Axon Regeneration into Growth-Permissive Transplants

Superior olivary contributions to auditory system plasticity: Medial but not lateral olivocochlear neurons are the source of cochleotomy‐induced GAP‐43 expression in the ventral cochlear nucleus

Contact Info

Product

Resources

About