GABA and glycine, the main neurotransmitters for adult spinal cord inhibitors, play a key role in neural plasticity. They can be excitors depending on the concentration of the target neurone chloride. This is mainly regulated by the co-carriers, KCC2, specific to neurons and NKCC1, ubiquitous. These proteins remove and enter the chloride ions respectively. During development, the expression of KCC2 increases while that of NKCC1 decreases, as the effect of post-synaptic inhibitor potentials on neuron membrane potential changes from depolarisation to hyperpolarisation. A medal injury at P0 blocks this developmental increase. This is correlated with a loss of KCC2 function, which is restored after treatment with a 5-HT2 receptor agonist, indicating that the descending routes from the brain trunk, in particular serotoninergic, are essential for the inhibitor system to mature. Injury in adults leads to a decrease in KCC2 expression, especially on the surface of the motoneurones and as a result in the strength of post-synaptic inhibition. BDNF is involved in this decrease but its effect is reversed 15 days after the injury, allowing the re-routing of KCC2 to the cell surface. Phosphorylation of tyrosins and sera is involved in addressing and stabilising KCC2 in the plasmic membrane, whereas threonins play a role in its functional activation. These results indicate that KCC2 is a target of choice to restore neural inhibition in the spinal cord after trauma.