| First Author | Gagliardini V | Year | 2000 |
| Journal | Mol Cell Neurosci | Volume | 16 |
| Issue | 1 | Pages | 27-33 |
| PubMed ID | 10882480 | Mgi Jnum | J:63793 |
| Mgi Id | MGI:1861582 | Doi | 10.1006/mcne.2000.0850 |
| Citation | Gagliardini V, et al. (2000) Absence of GAP-43 can protect neurons from death. Mol Cell Neurosci 16(1):27-33 |
| abstractText | The main function of GAP-43 is thought to be regulating growth cone motility and axon guidance signals. GAP-43 is highly expressed during development and in regenerating nerves and in particular regions of the adult brain. We here present the first evidence that GAP-43 can modulate guidance signals emanating from Semaphorin III (SemaIII) in cultured NGF-dependent sensory neurons. We further show that absence of GAP-43 dramatically increases resistance of specific sensory neurons to apoptotic stimuli in vitro. NGF-dependent sensory neurons from GAP-43 (+/-) and null mutant mice are strongly protected against SemaIII-induced death. Furthermore, NGF- and BDNF-dependent neurons, but not NT-3-dependent neurons, from GAP-43 null mutant mice are much more resistant to apoptosis induced by trophic factor deprivation. We also show that early postnatal Purkinje cells from GAP-43 (+/-) mice are more resistant to cell death in organotypic cultures. We conclude that GAP-43 can influence neuronal survival and modulate repulsive axon guidance signals. Copyright 2000 Academic Press. |
