A physical impact to spinal cord causes a temporary motor areflexia below lesion during the clinical phase known as spinal shock. Spinal shock remains a quite mysterious phenomenon mainly due to the lack of a consistent preclinical model to study the early functional consequences of injury without the inevitable use of anesthesia, which in turn affects spinal excitability. In this study, our custom-made micro impactor provides a calibrated impact to the ventral surface of the thoracic spinal cord of in vitro neonatal rat preparations of entire CNS. Ventral root (VR) recordings continuously traced dynamics of baseline spontaneous activities, and electrically-induced reflex responses before and after the injury from several spinal segments, simultaneously. Spinal impact elicited an immediate transient depolarization (15 min) that spread from the injury site to the rostral and caudal cord in ventro-dorsal directions and with distinct segmental velocities. A transient drop in tissue oxygen levels parallels the dynamics of injury-induced potentials. Stronger compressions induced higher peaks of potentials, with severe impacts completely disconnecting longitudinal tracts. Below the injury site, compressions suppressed lumbar fictive respiration and spontaneous bursting, and transiently halted electrically induced reflex responses that later completely recovered to control values. Moreover, low Cl- modified Krebs solution amplified the magnitude of injury potentials Overall, the novel in vitro platform traces early functional consequences of severe physical impacts that suppress rostro-caudal connectivity along the spinal cord. Resulting injury potentials spread away from the thoracic injury site, transiently suppress motor reflexes, and are sustained by low extracellular Cl- concentration.