Ultrastructural Analysis of Target-Dependent Properties of Mammalian Motoneurones
Mature motoneurones demonstrate a major dependence on the periphery for normal maintenance, as revealed through their retrograde response to axotomy, interruption of axonal transport, or blockade of neuromuscular transmission [8, 12, 20]. Likewise the immature motoneurone is dependent on a maintained functional contact with the muscle fibres it innervates for its differentiation and survival . Immature motoneurones die on losing contact with their muscle targets following motor nerve crush (i.e. axotomy; cf. ), while fully mature motoneurones survive under similar circumstances providing they regain functional contact with their targets following axonal regeneration . To investigate further this target-dependence of motoneurones, we have used the paradigm of reversible axotomy (nerve crush) or chronic axotomy (nerve section with proximal ligation) of intercostal nerves in adult cats to study changes in Nissl-body ultrastructure as a measure of altered protein synthesis. This approach follows our recent experience with the topographically distinct Nissl body that is located postsynaptically and immediately subjacent to the C-type synapse and its subsynaptic cistern [14, 15]. With the chronic partial central deafferentation that occurs following spinal hemisection, the presynaptic axon terminal of the C-type synapse selectively hypertrophies, and this presynaptic response is accompanied by an increase in size and a change in the ribosomal organisation of the postsynaptic Nissl body . Since the synthesis of particular classes of protein has been associated with particular forms of ribosomal organisation , functional correlates of altered protein synthesis can be inferred from changes in the ribosomal organisation of Nissl bodies. This approach has now been extended to the analysis of Nissl bodies sited in the general cytoplasm of normal and axotomised motoneurones.
KeywordsHydrate Cobalt Citrate Propylene Polypeptide
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- 2.Bearcroft CP, Lowrie MB, Peterson DC (1983) Selective effect of postnatal nerve crush on “fast” motor units in the rat. J Physiol (Loud) 338: 12 PGoogle Scholar
- 4.Hamburger V (1977) The developmental history of the motor neuron. Neurosci Prog Res Bull 15: 1–37Google Scholar
- 5.Ingoglia NA, Zanakis MF, Chakraborty G (1984) Transfer-RNA-mediated post-translational aminoacylation of proteins in axons. In: Elam JS, Cancalon P (eds) Axonal transport in neuronal growth and regeneration. Plenum, London (Advances in neurochemistry, vol 6, pp 119–136Google Scholar
- 6.Johnson IP (1983) Morphological correlates of altered protein synthesis: an ultrastructural analysis of axotomy and diphtheritic intoxication. PhD thesis, University of London, LondonGoogle Scholar
- 7.Johnson IP, Pullen AH, Sears TA (1986) Correlative optical and electronmicroscope analysis of Nissl body structure in cat thoracic motoneurones (to be published )Google Scholar
- 9.Lieberman AR (1974) Some factors affecting the retrograde responses to axonal lesions. In: Bellairs R, Gray EG (eds) Essays on the nervous system. Clarendon, Oxford, pp 71–105Google Scholar
- 15.Pullen AH, Sears TA (1983) Trophism between C-type axon terminals and thoracic moto-neurones in the cat. J Physiol (Load) 337: 373–388Google Scholar
- 16.Romanes GL (1946) Motor localisation and the effect of nerve injury on the ventral horn cells of the spinal cord. J Anat 80: 117–131Google Scholar
- 20.Watson WE (1969) The response of motor neurones to intramuscular injection of botulinum toxin. J Physiol (Lond) 202: 611–630Google Scholar
- 21.Willard M, Skene JHP (1982) Molecular events in axonal regeneration. In: Nicholls JG (ed) Repair and regeneration of the nervous system. Springer, Berlin Heidelberg New York (Dahlemer Konferenzen, pp 71–89Google Scholar
- 22.Willard M, Skene JHP, Simon C, Meiri K, Hirokawa N, Glicksman M (1984) Regulation of axon growth and cytoskeletal development. In: Elam JS, Cancalon P (eds) Axonal transport in neuronal growth and regeneration. Plenum, London (Advances in neurochemistry, vol 6, pp 171–183Google Scholar