The neuronal growth-associated protein GAP-43 (B-50, F1): neuronal specificity, developmental regulation and regional distribution of the human and rat mRNAs

Rl, Neve; Ni, Perrone-Bizzozero; Finklestein, Seth P.; Zwiers, H.; Bird, Edward D.; Dm, Kurnit; Benowitz, Larry I.

doi:10.1016/s0006-8993(87)80012-4

Cited by 60 publications

(42 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because it is extremely difficult to directly determine mRNA half-lives in vivo, an alternative method for inferring this measurement involves comparison of the steady-state levels of the primary and mature transcripts. To this end, we performed quantitative isotopic in situ hybridizations using two 35 S-radiolabeled riboprobes: one that recognizes exonic sequences in the GAP-43 gene (Neve et al 1987) and another that only recognizes sequences in the first intron (Namgung and Routtenberg 2000). In agreement with the results of previous studies (Namgung and Routtenberg 2000;Schauwecker et al 2000) no mature GAP-43 mRNA was detected in DGCs of control adult mice but high levels of this mRNA were seen in CA3 and CA1 regions (Fig.…”

Section: Effect Of Hud Overexpression In the Control Of Gap-43 Gene Esupporting

confidence: 84%

“…Sections (14 lm) were cut with a cryostat and stored at ) 80°C. Sections were hybridized overnight at 55°C with 1.5 · 10 6 cpm/100 lL or 4 · 10 6 cpm/100 lL of the specific 35 S-labeled riboprobes for mature GAP-43 mRNA (Neve et al 1987) and GAP-43 pre-mRNA (Namgung and Routtenberg 2000) respectively. After hybridization, sections were treated with RNase A, washed, and finally dehydrated with increasing concentrations of ethanol.…”

Section: Quantitative In Situ Hybridizationmentioning

confidence: 99%

See 1 more Smart Citation

In vivo post‐transcriptional regulation of GAP‐43 mRNA by overexpression of the RNA‐binding protein HuD

Bolognani

Tanner

Merhege

et al. 2006

Journal of Neurochemistry

View full text Add to dashboard Cite

HuD is a neuronal-specific RNA-binding protein that binds to and stabilizes the mRNAs of growth-associated protein-43 (GAP-43) and other neuronal proteins. HuD expression increases during brain development, nerve regeneration, and learning and memory, suggesting that this protein is important for controlling gene expression during developmental and adult plasticity. To examine the function of HuD in vivo, we generated transgenic mice overexpressing human HuD under the control of the calcium-calmodulin-dependent protein kinase IIa promoter. The transgene was expressed at high levels throughout the forebrain, including the hippocampal formation, amygdala and cerebral cortex. Using quantitative in situ hybridization, we found that HuD overexpression led to selective increases in GAP-43 mRNA in hippocampal dentate granule cells and neurons in the lateral amygdala and layer V of the neorcortex. In contrast, GAP-43 pre-mRNA levels were unchanged or decreased in the same neuronal populations.Comparison of the levels of mature GAP-43 mRNA and premRNA in the same neurons of transgenic mice suggested that HuD increased the stability of the transcript. Confirming this, mRNA decay assays revealed that the GAP-43 mRNA was more stable in brain extracts from HuD transgenic mice than non-transgenic littermates. In conclusion, our results demonstrate that HuD overexpression is sufficient to increase GAP-43 mRNA stability in vivo.

show abstract

Section: Effect Of Hud Overexpression In the Control Of Gap-43 Gene Esupporting

confidence: 84%

Section: Quantitative In Situ Hybridizationmentioning

confidence: 99%

In vivo post‐transcriptional regulation of GAP‐43 mRNA by overexpression of the RNA‐binding protein HuD

Bolognani

Tanner

Merhege

et al. 2006

Journal of Neurochemistry

View full text Add to dashboard Cite

show abstract

“…The sections were hybridized with 35S-GAP-43 or 35S-TPH riboprobes at 55°C for 16 hr. 35S labelled RNA probes were prepared through in vitro transcription of rat TPH cDNA subcloned in the pSP18 vector (TPH-1;Darmon et al, 1988) and of rat GAP-43 cDNA (clone GAllB; Neve et al, 1987) subcloned in pGEM 3. The full-length RNA probe of TPH, about 1.4 kb long, was hydrolyzed in order to obtain fragments of about 200 nucleotides.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Perinatal morphine treatment inhibits pruning effect and regeneration of serotoninergic pathways following neonatal 5,7‐HT lesions

Gorio

Giulio

Germani

et al. 1993

J of Neuroscience Research

View full text Add to dashboard Cite

Lesion of the serotoninergic system in neonate rats is an ideal model for assessing the activity of chemical substances capable of affecting neuronal plasticity and regeneration (Jonsson et al., Dev Brain Res 16: 171-180, 1984). Treatment of newborn rats within 6 hr from birth with the selective neurotoxin 5,7-dihydroxytryptamine causes degeneration of the most distal serotoninergic axons. In our experimental conditions we have observed that after such neurotoxic treatment there is spinal cord denervation, which is particularly remarkable in the lumbar segment. This degenerative event is followed by gradual regeneration of the lesioned axons, with good reinnervation of the entire cord within 8 weeks. The degeneration-regeneration process is correlated with a transient hyperinnervation of the pons-medulla and hypothalamus by the short collaterals (pruning effect), as evidenced by increased serotonin content. Perinatal morphine exposure markedly impairs serotonin regeneration in the spinal cord. In addition, opiate treated rats are more susceptible to lesions, as shown by the neurotoxin induced denervation of the cortex, pons-medulla, and hypothalamus, which does not occur in lesioned controls. Therefore, our observations suggest that perinatal exposure to morphine affects the plasticity and regeneration of the developing serotoninergic system by increasing its susceptibility to neurotoxic lesions and reducing its regenerative capacity.

show abstract

“…, 1989; De la Monte et af., 1989;Verhaagen et al, 1990a,b). In the adult human brain B-50/GAP43 is particularly abundant in associative areas of the neocortex (Neve et al, 1987;Ng et al, 1988). Following lesioning of peripheral nerve, high levels of B-50/GAP43 are associated with the newly formed regenerating fibers.…”

Section: Introductionmentioning

confidence: 99%

B‐50/GAP43 Expression Correlates with Process Outgrowth in the Embryonic Mouse Nervous System

Biffo

Verhaagen

Schrama

et al. 1990

Eur J of Neuroscience

112

View full text Add to dashboard Cite

The hypothesis that B-50/GAP43, a membrane-associated phosphoprotein, is involved in process outgrowth has been tested by studying the developmental pattern of expression of B-50/GAP43 mRNA and protein during mouse neuroembryogenesis. B-50/GAP43 mRNA is first detectable at embryonic day 8.5 (E8.5) in the presumptive acoustico-facialis ganglion. Subsequently, both B-50/GAP43 mRNA and protein were co-expressed in a series of neural structures: in the ventral neural tube (from E9.5) and dorsal root ganglia (from E10.5), in the marginal layer of the neuroepithelium surrounding the brain vesicles and in the cranial ganglia (from E9.5), in the autonomic nervous system (from E10.5), in the olfactory neuroepithelium and in the mesenteric nervous system (from E11.5), in a continuum of brain regions (from E12.5) and in the retina (from E13.5). Immunoreactive fibers were always seen arising from these regions when they expressed B-50/GAP43 mRNA. The spatial and temporal pattern of B-50/GAP43 expression demonstrates that this protein is absent from neuroblasts and consistently appears in neurons committed to fiber outgrowth. The expression of the protein in immature neurons is independent of their embryological origin. Our detailed study of B-50/GAP43 expression during mouse neuroembryogenesis supports the view that this protein is involved in a process common to all neurons elaborating fibers.

show abstract

The neuronal growth-associated protein GAP-43 (B-50, F1): neuronal specificity, developmental regulation and regional distribution of the human and rat mRNAs

Cited by 60 publications

References 0 publications

In vivo post‐transcriptional regulation of GAP‐43 mRNA by overexpression of the RNA‐binding protein HuD

In vivo post‐transcriptional regulation of GAP‐43 mRNA by overexpression of the RNA‐binding protein HuD

Perinatal morphine treatment inhibits pruning effect and regeneration of serotoninergic pathways following neonatal 5,7‐HT lesions

B‐50/GAP43 Expression Correlates with Process Outgrowth in the Embryonic Mouse Nervous System

Contact Info

Product

Resources

About