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 [4]. Immature motoneurones die on losing contact with their muscle targets following motor nerve crush (i.e. axotomy; cf. [2]), while fully mature motoneurones survive under similar circumstances providing they regain functional contact with their targets following axonal regeneration [16]. 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 [15]. Since the synthesis of particular classes of protein has been associated with particular forms of ribosomal organisation [11], 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.