Disuse-induced enhancement of Ia synaptic transmission in spinal motoneurons of the rat.

Monosynaptic excitatory postsynaptic potentials (EPSPs) evoked in rat spinal motoneurons by stimulation of a muscle nerve are enhanced during the first few days after section of the muscle nerve before subsiding to subnormal levels. We have examined whether this biphasic alteration results from changes of different factors involved in the regulation of central synaptic function. We chronically blocked the conduction of the intact peripheral nerve with tetrodotoxin (TTX). Under this disuse condition, enhancement of monosynaptic EPSPs was fully expressed within 2 d, and synaptic function remained elevated for at least 3 d, even after resumption of the impulse activity following discontinuance of the TTX. The magnitude of synaptic enhancement and the minimal period of nerve block required for synaptic enhancement were both comparable to those observed following nerve section. Thus, the early synaptic enhancement produced by section of the peripheral nerve could be accounted for entirely by the deprivation of sensory impulse activity. However, a prolonged nerve block up to 6 d still maintained synaptic enhancement. This was in contrast with synaptic depression observed after the first 3-4 d following section of the peripheral nerve. The late synaptic depression can thus be attributed to changes in some factors other than sensory impulse activity. Therefore, sensory impulse activity and the peripheral axonal continuity of sensory fibers appear to be 2 distinct factors for the regulation of central synaptic function.