Motor nerve injury results in a sequence of events known as Wallerian degeneration, which takes 1 - 2 days in rodents. Wallerian degeneration is significantly delayed in the naturally occurring C57BL/Wld^s mutant mouse. The ability to produce compound action potentials and the degradation of axonal material are delayed for up to 3 weeks following nerve injury. This thesis aims to examine the processes that occur after nerve section at NMJs of mutant Wld^s and normal mice. Functional morphological measurement of actively recycling synaptic vesicles at wild type nerve terminals using the vital dye FM1-43 indicated that the loss of the ability to recycle synaptic vesicles occurred within 24 hours, coinciding with disruption of neurofilament and SV2 proteins (stained using immunocytochemical methods). In contrast, the degeneration of nerve terminals in Wld^s mice following nerve injury was significantly delayed, and one initiated was further slowed, degeneration occurring between 3 and 10 days after axotomy. Furthermore, the morphological appearance of Wld^s nerve terminals after lesion differed greatly from that of degenerating wild type terminals. Wld^s terminals appeared to be retracting from the endplate region rather than simply degenerating. Electrophysiological recordings from degenerating junctions demonstrate that the delay of degeneration/withdrawal from nerve terminals of Wld^s mice is accompanied by a coincident loss of synaptic function: the average transmitter release was consistently reduced compared with the contralateral controls. These data indicate that, as in normal mice, the first structural change to take place after nerve injury in mutant Wld^s mice is the disruption of nerve terminals at the NMJ, accompanied by a concurrent decline in synaptic function. This thesis proposes that nerve terminal retraction in the mutant mouse is caused by a withdrawal mechanism similar to that observed during synapse elimination, a naturally occurring activity-dependant developmental phenomenon, rather than by classical Wallerian degeneration as previously assumed. To test this hypothesis, botulinum toxin (which abolishes neurotransmitter release) was administered to the nerve terminal region at the same time as the nerves were lesioned. The results indicate that nerve terminal withdrawal still occurs, but that it is reduced and further delayed in muscles treated with botulinum toxin by 2-3 days, in comparison with denervated alone Wld^s muscles.