Factors outside neuraxis mediate "acute" increase in EPSP amplitude caudal to spinal cord transection.

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Abstract
Experiments were undertaken to explore mechanisms responsible for the elevation in Ia-fiber .alpha.-motoneuron EPSP [excitatory postsynaptic potential] amplitude that occurs within hours of a spinal cord transection at a more rostral level. The spike-triggered averaging technique was used to record individual EPSP produced by single medial gastrocnemius (MG) Ia-fibers in MG motoneurons. In anesthetized cats spinal cord transection at a level (T13) rostral to the recording segment (L7-S1) causes no change in EPSP properties within the first 10-20 min. In cats with chronic spinal cord transection at T13, a 2nd transection at T11 causes enlargement of EPSP recorded in MG motoneurons within hours. The properties of EPSP in these doubly transected preparations differ in some details from those observed after a single acute transection. The finding that spinal cord transection at T11 can result in enlarged EPSP at L7-S1 in preparations previously transected at T13 indicates that spinal injury can influence synaptic transmission via pathways that are not totally contained within the neuraxis. Spinal cord transection consistently yields a greater enlargement of EPSP recorded in small motoneurons than those in large ones. Large motoneurons participate only when the increase exhibited in the small ones is relatively large.