The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review


Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Axotomy


High impact information on Axotomy


Chemical compound and disease context of Axotomy


Biological context of Axotomy

  • Downregulation of Na(v)1.9, which results from a lack of peripheral glial cell-derived neurotrophic factor following peripheral axotomy, might retune DRG neurons and contribute to their hyperexcitability after nerve injury [16].
  • Apoptosis resulting from normal development or from axotomy can be inhibited markedly by exogenous neuregulin [17].
  • Because these results raised the possibility that axonal loss may influence neurotrophin expression only in SCs that have differentiated toward a myelinating phenotype, we measured BDNF mRNA after axotomy in the cervical sympathetic trunk (CST), a predominantly unmyelinated autonomic nerve [18].
  • Changes in the synthesis and axonal transport of neurofilament (NF) proteins and tubulin were examined after various selective axotomies of adult rat DRG cells [19].
  • Removal of NT-3 4-5 weeks after beginning treatment resulted in a decline of conduction velocity and EPSP amplitude within 1 week to values characteristic of axotomy [20].

Anatomical context of Axotomy


Associations of Axotomy with chemical compounds

  • These results suggest that transient activation of PKC, PKA, and/or serine phosphatase inhibition by axotomy triggers persistent intracellular changes that may be related to polarity loss in these neurons [26].
  • Taken together, these findings suggest that activation of c-Jun mediates the loss of dopamine neurons after axotomy injury [27].
  • Axotomy induces the expression of vasopressin receptors in cranial and spinal motor nuclei in the adult rat [28].
  • M-35 potentiated the facilitation of the flexor reflex by conditioning stimulation of cutaneous unmyelinated afferents in rats with intact nerves and the potentiating effect of M-35 on the conditioning-stimulation-induced reflex facilitation of the cutaneous unmyelinated afferents was strongly enhanced after axotomy [29].
  • Administration of testosterone attenuates neuronal loss following axotomy in the brain-stem motor nuclei of female rats [30].

Gene context of Axotomy

  • In vivo, CT-1 protected neonatal sciatic motoneurons against the effects of axotomy [31].
  • BDNF and NT-4/5 prevent atrophy of rat rubrospinal neurons after cervical axotomy, stimulate GAP-43 and Talpha1-tubulin mRNA expression, and promote axonal regeneration [32].
  • In newborn animals in which CNTF is not yet expressed, exogenous CNTF that is locally administered very effectively protects motoneurons from degeneration by axotomy [33].
  • In a sciatic axotomy model of neuronal injury in the neonate, death of DRG neurons was also reduced by JNK3 deficiency [34].
  • Administration of nerve growth factor (NGF) rescued the immunoreactivity of substance P, which is known to disappear after peripheral axotomy, but not influence that of both E-cadherin or alpha N-catenin [35].

Analytical, diagnostic and therapeutic context of Axotomy


  1. Muscarinic receptor binding and oxidative enzyme activities in the adult rat superior cervical ganglion: effects of 6-hydroxydopamine and nerve growth factor. Dombrowski, A.M., Jerkins, A.A., Kauffman, F.C. J. Neurosci. (1983) [Pubmed]
  2. Flunarizine improves the survival of grafted dopaminergic neurons. Kaminski Schierle, G.S., Hansson, O., Brundin, P. Neuroscience (1999) [Pubmed]
  3. Streptozotocin-induced diabetes mellitus causes changes in primary sensory neuronal cytoskeletal mRNA levels that mimic those caused by axotomy. Liuzzi, F.J., Bufton, S.M., Vinik, A.I. Exp. Neurol. (1998) [Pubmed]
  4. Spinal axonal injury transiently elevates the level of metabotropic glutamate receptor 5, but not 1, in cord-projection central neurons. Wang, Y.J., Tseng, G.F. J. Neurotrauma (2004) [Pubmed]
  5. Prevention of motoneuron death by adenovirus-mediated neurotrophic factors. Giménez y Ribotta, M., Revah, F., Pradier, L., Loquet, I., Mallet, J., Privat, A. J. Neurosci. Res. (1997) [Pubmed]
  6. In vivo neurotrophic effects of GDNF on neonatal and adult facial motor neurons. Yan, Q., Matheson, C., Lopez, O.T. Nature (1995) [Pubmed]
  7. Ciliary neurotrophic factor prevents the degeneration of motor neurons after axotomy. Sendtner, M., Kreutzberg, G.W., Thoenen, H. Nature (1990) [Pubmed]
  8. Flunarizine protects neurons from death after axotomy or NGF deprivation. Rich, K.M., Hollowell, J.P. Science (1990) [Pubmed]
  9. Nerve growth factor treatment after brain injury prevents neuronal death. Kromer, L.F. Science (1987) [Pubmed]
  10. Can galanin also be considered as growth-associated protein 3.2? Zigmond, R.E. Trends Neurosci. (2001) [Pubmed]
  11. Differential effects of axotomy on substance P-containing and nicotinic acetylcholine receptor-containing retinal ganglion cells: time course of degeneration and effects of nerve growth factor. Ehrlich, D., Keyser, K., Manthorpe, M., Varon, S., Karten, H.J. Neuroscience (1990) [Pubmed]
  12. Sensory neuroprotection, mitochondrial preservation, and therapeutic potential of N-acetyl-cysteine after nerve injury. Hart, A.M., Terenghi, G., Kellerth, J.O., Wiberg, M. Neuroscience (2004) [Pubmed]
  13. No overlap of sensitivity to capsaicin and expression of galanin in rat dorsal root ganglion neurons after axotomy. Wendland, J.R., Schmidt, K.H., Koltzenburg, M., Petersen, M. Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. (2003) [Pubmed]
  14. Kainic acid destroys displaced amacrine cells in post-hatch chicken retina. Ehrlich, D., Morgan, I.G. Neurosci. Lett. (1980) [Pubmed]
  15. Failure to activate NF-kappaB promotes apoptosis of retinal ganglion cells following optic nerve transection. Choi, J.S., Kim, J.A., Kim, D.H., Chun, M.H., Gwag, B.J., Yoon, S.K., Joo, C.K. Brain Res. (2000) [Pubmed]
  16. NaN/Nav1.9: a sodium channel with unique properties. Dib-Hajj, S., Black, J.A., Cummins, T.R., Waxman, S.G. Trends Neurosci. (2002) [Pubmed]
  17. Axonal interactions regulate Schwann cell apoptosis in developing peripheral nerve: neuregulin receptors and the role of neuregulins. Grinspan, J.B., Marchionni, M.A., Reeves, M., Coulaloglou, M., Scherer, S.S. J. Neurosci. (1996) [Pubmed]
  18. A distinct pattern of trophic factor expression in myelin-deficient nerves of Trembler mice: implications for trophic support by Schwann cells. Friedman, H.C., Jelsma, T.N., Bray, G.M., Aguayo, A.J. J. Neurosci. (1996) [Pubmed]
  19. Axotomy-induced alterations in the synthesis and transport of neurofilaments and microtubules in dorsal root ganglion cells. Oblinger, M.M., Lasek, R.J. J. Neurosci. (1988) [Pubmed]
  20. Neurotrophin modulation of the monosynaptic reflex after peripheral nerve transection. Mendell, L.M., Johnson, R.D., Munson, J.B. J. Neurosci. (1999) [Pubmed]
  21. Mutant SOD1 causes motor neuron disease independent of copper chaperone-mediated copper loading. Subramaniam, J.R., Lyons, W.E., Liu, J., Bartnikas, T.B., Rothstein, J., Price, D.L., Cleveland, D.W., Gitlin, J.D., Wong, P.C. Nat. Neurosci. (2002) [Pubmed]
  22. Retrograde axonal transport of LIF is increased by peripheral nerve injury: correlation with increased LIF expression in distal nerve. Curtis, R., Scherer, S.S., Somogyi, R., Adryan, K.M., Ip, N.Y., Zhu, Y., Lindsay, R.M., DiStefano, P.S. Neuron (1994) [Pubmed]
  23. Ninjurin, a novel adhesion molecule, is induced by nerve injury and promotes axonal growth. Araki, T., Milbrandt, J. Neuron (1996) [Pubmed]
  24. Interleukin 3 as a trophic factor for central cholinergic neurons in vitro and in vivo. Kamegai, M., Niijima, K., Kunishita, T., Nishizawa, M., Ogawa, M., Araki, M., Ueki, A., Konishi, Y., Tabira, T. Neuron (1990) [Pubmed]
  25. Leukemia inhibitory factor mediates an injury response but not a target-directed developmental transmitter switch in sympathetic neurons. Rao, M.S., Sun, Y., Escary, J.L., Perreau, J., Tresser, S., Patterson, P.H., Zigmond, R.E., Brulet, P., Landis, S.C. Neuron (1993) [Pubmed]
  26. Axotomy-induced neurofilament phosphorylation is inhibited in situ by microinjection of PKA and PKC inhibitors into identified lamprey neurons. Hall, G.F., Kosik, K.S. Neuron (1993) [Pubmed]
  27. c-Jun mediates axotomy-induced dopamine neuron death in vivo. Crocker, S.J., Lamba, W.R., Smith, P.D., Callaghan, S.M., Slack, R.S., Anisman, H., Park, D.S. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  28. Axotomy induces the expression of vasopressin receptors in cranial and spinal motor nuclei in the adult rat. Tribollet, E., Arsenijevic, Y., Marguerat, A., Barberis, C., Dreifuss, J.J. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  29. Galanin-mediated control of pain: enhanced role after nerve injury. Wiesenfeld-Hallin, Z., Xu, X.J., Langel, U., Bedecs, K., Hökfelt, T., Bartfai, T. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  30. Administration of testosterone attenuates neuronal loss following axotomy in the brain-stem motor nuclei of female rats. Yu, W.H. J. Neurosci. (1989) [Pubmed]
  31. Cardiotrophin-1, a cytokine present in embryonic muscle, supports long-term survival of spinal motoneurons. Pennica, D., Arce, V., Swanson, T.A., Vejsada, R., Pollock, R.A., Armanini, M., Dudley, K., Phillips, H.S., Rosenthal, A., Kato, A.C., Henderson, C.E. Neuron (1996) [Pubmed]
  32. BDNF and NT-4/5 prevent atrophy of rat rubrospinal neurons after cervical axotomy, stimulate GAP-43 and Talpha1-tubulin mRNA expression, and promote axonal regeneration. Kobayashi, N.R., Fan, D.P., Giehl, K.M., Bedard, A.M., Wiegand, S.J., Tetzlaff, W. J. Neurosci. (1997) [Pubmed]
  33. Endogenous ciliary neurotrophic factor is a lesion factor for axotomized motoneurons in adult mice. Sendtner, M., Götz, R., Holtmann, B., Thoenen, H. J. Neurosci. (1997) [Pubmed]
  34. c-Jun N-terminal kinase 3 deficiency protects neurons from axotomy-induced death in vivo through mechanisms independent of c-Jun phosphorylation. Keramaris, E., Vanderluit, J.L., Bahadori, M., Mousavi, K., Davis, R.J., Flavell, R., Slack, R.S., Park, D.S. J. Biol. Chem. (2005) [Pubmed]
  35. Alteration of E-cadherin and alpha N-catenin immunoreactivity in the mouse spinal cord following peripheral axotomy. Seto, A., Hasegawa, M., Uchiyama, N., Yamashima, T., Yamashita, J. J. Neuropathol. Exp. Neurol. (1997) [Pubmed]
  36. Axotomy upregulates the anterograde transport and expression of brain-derived neurotrophic factor by sensory neurons. Tonra, J.R., Curtis, R., Wong, V., Cliffer, K.D., Park, J.S., Timmes, A., Nguyen, T., Lindsay, R.M., Acheson, A., DiStefano, P.S. J. Neurosci. (1998) [Pubmed]
  37. Changes in the regulatory effects of cell-cell interactions on neuronal AChR subunit transcript levels after synapse formation. Levey, M.S., Jacob, M.H. J. Neurosci. (1996) [Pubmed]
  38. Localized and transient elevations of intracellular Ca2+ induce the dedifferentiation of axonal segments into growth cones. Ziv, N.E., Spira, M.E. J. Neurosci. (1997) [Pubmed]
  39. Leukemia inhibitory factor induces sympathetic sprouting in intact dorsal root ganglia in the adult rat in vivo. Thompson, S.W., Majithia, A.A. J. Physiol. (Lond.) (1998) [Pubmed]
  40. Coexpression patterns of mGLuR mRNAs in rat retinal ganglion cells: a single-cell RT-PCR study. Tehrani, A., Wheeler-Schilling, T.H., Guenther, E. Invest. Ophthalmol. Vis. Sci. (2000) [Pubmed]
WikiGenes - Universities