SEMINAR: Target-dependence of motoneurones

The Speaker: Ian obtained a BSc (hons) in anatomy in 1976 from the University of Birmingham and a PhD in neuroanatomy in 1983 from the Institute of Neurology, University of London. His postdoctoral work at the Institute of Neurology, London was concerned with the target-dependence of motoneurones. He was appointed senior lecturer in anatomy at the Royal Free and University College Medical School, London where he co-ordinated medical anatomy and worked on developing a strategy for neuronal rescue through gene transfer of IGF-1 isoforms. After two years as head of research at the McTimoney Chiropractic College in Oxfordshire, he moved in 2009 to the University of Adelaide. He is currently senior lecturer in the Discipline of Anatomy and Pathology where he researches mechanisms underlying neuronal injury and repair, and teaches anatomy, neuroscience and pathophysiology.

The Seminar: While it is known that immature motoneurone require contact with their muscle targets for maintenance and survival, little is known about the target-dependence of mature motoneurones. We have used peripheral axotomy as a means of perturbing motoneurone-target interactions to study this in neonatal, adult and ageing animals. This seminar will review data showing that:

1.The response of motoneurones to injury in adult and ageing animals is similar. 2.Diet restriction causes non-injured motoneuronal loss in aged animals and reduces the extent of motoneuronal loss after avulsion. 3.An isoform of IGF-1 expressed by stretched muscle is more effective in the rescue of adult motoneurones from avulsion-induced death than the liver-type isoform of IGF-1. Preliminary data indicate the opposite is true for neonatal motoneurones.

These findings call into question some commonly-held assumptions about ageing motoneurones that have traditionally been based on data obtained from studies of the immature neuromuscular system. This may be relevant to human age-related neurodegenerative conditions, such as Motor Neurone Disease.