Spinal cord injury (SCI) is manifested by pathologic changes in the areas significantly distant from the area of primary injury. In order to find new potential therapeutic targets to restore motor function, it is particularly relevant to identify the causes and mechanisms of these shifts in the lumbar spinal cord when injury occurs in the proximal spinal cord. On the model of dosed SCI the expression of Ca-binding protein parvalbumin (PARV), osteopontin (OPN) and glypican 4 (GPC4) in neurons of laminae VII, VIII and IX within segments L3–4 on 7 and 60 days of the experiment was studied. Laminas VII and IX show a decrease in the number of PARV+ neurons during the acute and chronic phase of SCI, which may indicate a decrease in calcium binding in ventral horn neurons at the level of segments L3–4. Decreased PARV expression in these neurons indicates an increased risk of their vulnerability and impaired motor function. The pattern of OPN expression in lumbar horn neurons distant from the epicenter of traumatic injury was studied for the first time. In all the studied laminae in the ventral horns of the gray matter, we did not observe shifts in the number of OPN+ neurons both in the acute and chronic phases of SCI. In lamina IX of the lumbar spinal cord, we found an increase in the number of GPC4+ neurons in the acute posttraumatic period, which can be regarded as a key positive adaptive reaction of neurons in the lumbar spinal cord remote from the epicenter of injury. The assessment of this reaction as positive is based on the data on the binding of GPC4 anchored on the neuron surface to various molecules with neuroprotective activity and stimulating neuroregeneration.