Lesioning alters functional properties in isolated spinal cord hemisegmental networks.

Hemisegmental networks produced by longitudinal lesions of the spinal cord midline are able to generate rhythmic bursting activity. This has led to the suggestion that hemisegmental networks can independently burst in the intact spinal cord. Previous analyses in the lamprey spinal cord failed to show hemisegmental bursting in NMDA. This was subsequently attributed to the failure to wait sufficient time for NMDA-evoked hemisegmental activity to recover after being abolished by the lesion, which can take tens of minutes to hours. The reason for this delay in the onset of NMDA-evoked activity was not previously addressed. We have investigated it here by examining two hypotheses: that hemisegmental networks intrinsically burst under normal conditions but that NMDA-evoked bursting was temporarily silenced by lesion-induced transmitter release; or that lesioning altered functional properties in the hemisegment that subsequently led to the development of bursting. We found no evidence to support transmitter-induced silencing of ongoing NMDA-evoked hemisegmental activity, but did find evidence for significant changes in the cellular and synaptic properties of motor neurons and premotor excitatory interneurons in lesioned hemisegmental networks. These results thus suggest that there are lesion-induced changes in functional properties in hemisegmental networks. As the interpretation of lesion studies rests on the assumption that the functional properties of hemisegmental components are not altered, further work is needed before conclusions can be made about the function of the intact system.