Traumatic spinal cord injuries result from mechanical damage followed by inflammation due to biochemical processes, which involves increased activity of astrocytes and macrophages, leading to cell death and loss of function. Recent studies have linked \(\alpha \) -synuclein ( \(\alpha \) -syn) expression to increased macrophage accumulation and astrocytes hyperactivity in the injured spinal cord of both humans and rodents. This study aimed to analyze the association between \(\alpha \) -syn and astrocyte and macrophage immunoreactivity in acute and chronic post-injury phases in rats. To examine this, two rats underwent a T9 mid-thoracic injury and cross-sections of the spinal cord from rats euthanized on the 1st and 21st postoperative days were immunolabeled for \(\alpha \) -syn, astrocytes, and macrophages (using GFAP and CD68 markers). The cell density was determined using ImageJ and Ilastik softwares. As results, \(\alpha \) -syn accumulated in profiles resembling astrocytes and between the cells in the white matter along the acute and chronic phases, although without significance. In the chronic phase, an increase in the cell density for GFAP (p < 0,05) and CD68 was identified in the fascicles gracilis and the dorsal corticospinal tract, in contrast to the high density of \(\alpha \) -syn and a decrease of neurons number in the motor pools. The findings highlight how the inflammatory cascade that persists in the chronic phase and mainly affects the dorsal ascending pathways and the dorsal corticospinal tract may be associated with an increase in \(\alpha \) -syn and a decrease in neuron density in the spinal gray matter.