Synaptic Loss from Axotomised α- and γ-Motoneurones

Abstract

Loss of synaptic terminals from the cell bodies of α-motoneurones within about a week of axotomy is well-documented (Blinzinger & Kreutzberg, 1968; Chen, 1978). Such loss may be due to the loss of peripheral target contact, since it also occurs after the interruption of axonal transport in peripheral nerves and when neuromuscular transmission is blocked (Cull, 1975; Sumner, 1979). Previously (Johnson, Pullen & Sears, 1990), we reported that the restoration of peripheral target contact is associated with the return towards normal of synaptic terminals contacting cat thoracic a-motoneurones. No such restoration occurred for motoneurones prevented from reinnervating muscle and we suggested that this difference reflected the influence of the peripheral target on the synapses contacting α-motoneurones. There is no information on the long-term effects of axotomy on the synapses of γ-motoneurones, although axotomy-induced changes in their central connectivity are also likely to affect the degree to which recovery of movement control occurs. In this study, therefore, we have compared the long-term effects of reversible- or permanent- axotomy on the synaptic terminals of α- and γ-motoneurones to determine the extent to which axotomy-induced changes are modified by the restoration of peripheral target contact.