A better understanding how therapeutic intervention affects the molecular and cellular post-traumatic processes may help to improve the functional repair after the spinal cord injury (SCI). It is known that the cellular concentrations of anti-oxidant dipeptide carnosine can be easily increased in dose-dependent manner by food or nutrition supplements. Current study investigated the effect of six-week carnosine treatments on cellular expressions of brain- and glial cell line-derived neurotrophic factors (BDNF, GDNF) following contusion SCI. In contrast to naïve control group, the SCI caused the reductions of BDNF and GDNF protein concentrations below as well above the thoracic SCI. However, in all injured rats, the mRNAs of neurotrophins were upregulated in the lumbar, but downregulated in the cervical enlargements. In contrast to injury model (IM) rats, carnosine significantly increased the BDNF, but reduced the GDNF mRNAs in the lumbar enlargement. The cellular correlation analyses showed the positive association between the microglial CX3C-motif- chemokine receptor-1 (CX3CR1) and both neurotrophins mRNAs in both injured groups. However, the positive correlations between the neurotrophins and astrocyte Glial fibrillary acidic protein (GFAP) and fibroblast Collagen 6 mRNAs were only found in the non-treated IM rats. In contrast to naïve control and carnosine-treated rats, the oligodendrocyte Olig2 mRNA was significantly decreased in the lumbar and neuronal nitric oxide synthase (nNOS) in the cervical enlargements of IM group. Current study demonstrated the carnosine effect on all glial cells. Furthermore, the carnosine treatment showed a neuroprotective effect on cervicolumbar nNOS connections.Supported by VEGA-2/0117/24