Advertisement

Motor Neurone Disease Research — Selection and Evaluation of Model Neurones

  • A. B. Mccruden
  • P. W. Schuetz
  • F. Tebling
Chapter
Part of the Keynes Seminars book series (KESE)

Abstract

The most remarkable feature of motor neurone disease (MND) is that it is virtually confined to the voluntary motor system. Its specificity of attack is not seen in any other disease of the nervous system (Appel, 1981). One hundred and fifty years after the condition was first described, little is known about its aetiology (Munsat et al., 1984). For example, particular groups of motor cells are spared at either end of the spinal column (controlling eye movement and the rectal sphincters, respectively), a phenomenon which has not been explained. The limited data on nerve cell physiology has allowed Weiner (1980) to suggest that this may be based on a difference in sensitivity towards androgenic hormones, receptors for which are found only on the cells which succumb to the disease. This hypothesis may not be correct, but there must be some biochemical or physiological basis to the selectivity. Others have suggested a toxic environmental factor as being responsible for MND (Yoshimasu et al., 1982). Detailed examination of motor neurones themselves may help to answer these questions.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Appel, S. H. (1981). A unifying hypothesis for the cause of amyotrophic lateral sclerosis, Parkinsonism, and Alzheimer disease. Ann. Neurol., 1, 499–505.CrossRefGoogle Scholar
  2. Dribin, L. B. and Barrett, J. N. (1980). Conditioned medium enhances neuritic outgrowth from rat spinal cord explants. Dev. Biol., 74, 184–195.CrossRefGoogle Scholar
  3. Galfre, G. and Milstein, C. (1981). Preparation of monoclonal antibodies: strategies and procedures. Meth. Enzymol., 73, 1–46.Google Scholar
  4. Gillespie, J. S., Hamilton, D. N. and Hosie, R. J. (1970). The extraneural uptake and localisation of noradrenaline in the cat spleen and the effect on this of some drugs. J. Physiol., 206, 563–590.CrossRefGoogle Scholar
  5. Hamill, O. P. and Sackmann, B. (1981). Multiple conductance states of single acetylcholine receptor channels in embryonic muscle cells. Nature, 294, 462–464.CrossRefGoogle Scholar
  6. Kobayashi, Y., Higuchi, M. and Osawa, T. (1982). Human T-cell hybridomas producing lymphokines. J. Immun., 128, 2714–2718.Google Scholar
  7. Littlefield, J. W. (1964). Selection of hybrids from matings of fibroblasts in vitro and their presumed recombinants. Science, 145, 709–710.CrossRefGoogle Scholar
  8. Munsat, T. L., Hedlund, W., Felmus, M., Cooper, C. and Gabbai, A. (1984). Clinical clues to the cause of amyotrophic lateral sclerosis, in G. Serratrice (ed.), Neuromuscular Diseases, Raven Press, New York, pp. 329–333.Google Scholar
  9. Nelson, P. G., Christian, C. N. and Nirenberg, M. W. (1976). Synapse formation between clonal neuroblastoma x glioma hybrid cells and striated muscle. Proc. natn. Acad. Sci. US, 73, 123–127.CrossRefGoogle Scholar
  10. Schuetz, P. W. and McCruden, A. B. (1985). Morphological differentiation of PC12 induced by NG108CC15 conditioned medium. Eur. J. Cell Biol., 36(8), 18.Google Scholar
  11. Smith, R. G. and Appel, S. H. (1983). Extracts of skeletal muscle increase neurite outgrowth and cholinergic activity of foetal rat spinal motor neurones. Science, 219, 1079–1081.CrossRefGoogle Scholar
  12. Weiner, L. P. (1980). Possible role of androgen receptors in amyotrophic lateral sclerosis. Arch. Neurol., 37, 129–131.CrossRefGoogle Scholar
  13. Yoshimasu, F., Yasui, M., Yase, Y., Uebayashi, Y. and Tanaka, S. (1982). Amyotrophic lateral sclerosis: distribution of metals in spinal cord tissue. Clin. Neurol., 22, 323–328.Google Scholar
  14. Zimmermann, U. (1982). Electric field-mediated fusion and related electrical phenomena. Biochim. Biophys. Ada, 694, 227–277.CrossRefGoogle Scholar

Copyright information

© Bioengineering Unit, University of Strathclyde 1988

Authors and Affiliations

  • A. B. Mccruden
  • P. W. Schuetz
  • F. Tebling

There are no affiliations available

Personalised recommendations