Effect of proximal axotomy on GAP-43 expression in cortical neurons in the mouse

Elliott, Ellen J.; Parks, Deborah A.; Fishman, Paul S.

doi:10.1016/s0006-8993(97)00100-5

Cited by 18 publications

(16 citation statements)

References 30 publications

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“…(3) Death becomes a prominent cellular response at later intervals after injury, further complicating interpretation of regeneration related changes. In previous work, we found that transcallosal neurons in the mouse did not upregulate GAP-43 mRNA following axotomy 1-2 mm from the cell body (Elliott et al, 1997), consistent with the minimal axonal sprouting seen after injury. In this study, we have sought to determine whether mouse transcallosal neurons fail to respond to injury that is extremely proximal (only a few hundred microns away from the cell body), and whether the failure extends generally to other growth-associated proteins besides GAP-43.…”

Section: Introductionsupporting

confidence: 82%

“…Cortical pyramidal neurons that project across the corpus callosum were labeled by retrograde uptake of the fluorescent dye Fluoro-Gold, as described previously (Elliott et al, 1997). This procedure involves placing a dye soaked gelatin sponge over the fronto-parietal cortex of one hemisphere, and labels a large number of transcallosally projecting neurons that reside in the homotypic contralateral cortex (Fig.…”

Section: Methodsmentioning

confidence: 99%

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α₁-Tubulin Expression in Proximally Axotomized Mouse Cortical Neurons

Elliott

Parks²,

Fishman³

1999

Journal of Neurotrauma

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This paper further characterizes the response to axotomy of mouse transcallosal cortical neurons, a population of neurons that seems to be particularly refractory to regeneration. Mouse transcallosal cortical neurons did not upregulate mRNA for the growth-associated protein alpha 1-tubulin following axotomy, even when the axonal distance from injury to cell body was only 100-300 microns. Previous experiments had found no upregulation of another growth-associated protein, GAP-43, by transcallosal neurons following axotomy 1-2 mm from the cell body. These latest results establish that this population of neurons fails to respond to axotomy even when it is extremely proximal and that this failure is not a peculiarity specific to one growth-associated protein but is indicative of a generally poor regenerative response.

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Section: Introductionsupporting

confidence: 82%

Section: Methodsmentioning

confidence: 99%

α₁-Tubulin Expression in Proximally Axotomized Mouse Cortical Neurons

Elliott

Parks²,

Fishman³

1999

Journal of Neurotrauma

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“…To study the progesterone effects on GAP-43 mRNA during the three stage periods, we employed in situ hybridization (ISH) using a synthetic 35 S-oligonucleotide probe complementary to GAP-43 mRNA (Elliott et al 1997). Probe signal in NFR/NFR mice with or without progesterone treatment was low, as shown in the semiquantitative grain counting of Fig.…”

Section: Resultsmentioning

confidence: 99%

“…A synthetic oligonucleotide probe with the sequence 5 0 -CGCAGCCTTATGAGCCTTATCTTCCGGC TTGACACCATC-3 0 (Elliott et al 1997) was end labeled with ( 35 S)-ATP using the enzyme terminal transferase. For ISH, mice were transcadially perfused with 4% PFA prepared in diethylpirocarbonate-treated water.…”

Section: Choline Acetyltransferase Glial Fibrillary Acidic Protein Amentioning

confidence: 99%

Stage Dependent Effects of Progesterone on Motoneurons and Glial Cells of Wobbler Mouse Spinal Cord Degeneration

et al. 2009

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In the Wobbler mouse, a mutation in the Vps54 gene is accompanied by motoneuron degeneration and astrogliosis in the cervical spinal cord. Previous work has shown that these abnormalities are greatly attenuated by progesterone treatment of clinically afflicted Wobblers. However, whether progesterone is effective at all disease stages has not yet been tested. The present work used genotyped (wr/wr) Wobbler mice at three periods of the disease: early progressive (1-2 months), established (5-8 months) or late stages (12 months) and age-matched wildtype controls (NFR/NFR), half of which were implanted with a progesterone pellet (20 mg) for 18 days. In untreated Wobblers, degenerating vacuolated motoneurons were initially abundant, experienced a slight reduction at the established stage and dramatically diminished during the late period. In motoneurons, the cholinergic marker choline acetyltransferase (ChAT) was reduced at all stages of the Wobbler disease, whereas hyperexpression of the growth-associated protein (GAP43) mRNA preferentially occurred at the early progressive and established stages. Progesterone therapy significantly reduced motoneuron vacuolation, enhanced ChAT immunoreactive perikarya and reduced the hyperexpression of GAP43 during the early progressive and established stages. At all stage periods, untreated Wobblers showed high density of glial fibrillary acidic protein (GFAP)+ astrocytes and decreased number of glutamine synthase (GS) immunostained cells. Progesterone treatment down-regulated GFAP+ astrocytes and up-regulated GS+ cell number. These data reinforced the usefulness of progesterone to improve motoneuron and glial cell abnormalities of Wobbler mice and further showed that therapeutic benefit seems more effective at the early progressive and established periods, rather than on advance stages of spinal cord neurodegeneration.

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“…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

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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.

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Effect of proximal axotomy on GAP-43 expression in cortical neurons in the mouse

Cited by 18 publications

References 30 publications

α₁-Tubulin Expression in Proximally Axotomized Mouse Cortical Neurons

α₁-Tubulin Expression in Proximally Axotomized Mouse Cortical Neurons

Stage Dependent Effects of Progesterone on Motoneurons and Glial Cells of Wobbler Mouse Spinal Cord Degeneration

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

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Effect of proximal axotomy on GAP-43 expression in cortical neurons in the mouse

Cited by 18 publications

References 30 publications

α1-Tubulin Expression in Proximally Axotomized Mouse Cortical Neurons

α1-Tubulin Expression in Proximally Axotomized Mouse Cortical Neurons

Stage Dependent Effects of Progesterone on Motoneurons and Glial Cells of Wobbler Mouse Spinal Cord Degeneration

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

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α₁-Tubulin Expression in Proximally Axotomized Mouse Cortical Neurons

α₁-Tubulin Expression in Proximally Axotomized Mouse Cortical Neurons