In the vast majority of injuries to the spinal cord, the neuronal circuits responsible for locomotion, located in the lumbar region, are not directly impaired by the primary damage although they may result more or less completely disconnected from the supraspinal centers due to the severance of the fibers passing across the lesion site.

In the present study, we have investigated how the lumbar locomotor networks are affected by a focal lesion involving only few spinal segments above.

For this purpose, we applied a toxic solution (recently developed in our laboratory) that mimics the principal factors responsible for the secondary injury and that we named pathological medium plus kainate (indicated as PM + KA).

We have reported that PM + KA, if applied to the whole spinal cord, is able to reproduce the histological and functional outcomes of a spinal cord lesion. The functional consequences are monitored for up to 24 hours by recording from ventral roots the reflex responses as well as the presence of locomotor-like oscillatory cycles. At the end of the experiments, samples were fixed for histological analysis.

Preliminary experiments confirm that the experimental procedures needed for limiting the lesion did not damage spinal cord activity.

In the current experiments, while PM + KA (applied focally) acted on only few segments located in the thoracic region, spinal neurons in remote segments showed simultaneous depolarization that eventually faded away to pre treatment baseline.

The efficacy of synaptic transmission was recorded above, within and below the lesion site, while the activity of locomotor circuits in the lumbar portion was measured by eliciting a fictive locomotion rhythm with neurochemicals or trains of repetitive stimuli to dorsal root afferents.

A limited number of surviving axons crossing the injured portions could still functionally connect segments above and below the lesion with appropriate electrical stimuli.

After the lesioning procedures, the operativity of lumbar networks, despite the minimal cell damage to the areas not directly exposed to the toxic, was impaired: chemically and electrically induced fictive locomotion was differentially affected by the lesion.

In fact, while the alternated oscillations elicited by neurochemicals, after a transient early suppression, could reappear following extensive wash out, the dorsal root elicited ones were completely and irreversibly lost.

The amplitude of the cumulative depolarization evoked by trains of repetitive stimuli was comparable for both post-lesional and control preparations, but responses summed up at a significantly lower speed, that was unable to trigger alternating oscillations.

The present study casts light on the very first events that alter the locomotor circuits following an experimental spinal cord injury.

The present data might have relevant implications for neurorehabilitation targeted to exploit the residual automatic capacity of the lumbar networks to gain functional benefits for spinal cord injured persons.