For in vivo intracellular recording in the adult spinal cord, larger animals have traditionally been used due to the stability needed for intracellular penetrations with fine electrodes and the robustness of the preparation to withstand the surgical procedures. To be able to take advantage of the developments in transgenic mice to understand both normal spinal function and its dysfunction in disease we successfully developed a laboratory capable of intracellular recording from identified spinal motoneurones in the adult mouse in vivo. Using this we identified key intrinsic properties of mice motoneurones. We then extended the model to include a decerebrate preparation and compared this with different anaesthesias. Using the decerebrate in vivo model we also demonstrated that is it possible to pharmacologically activate spinal central pattern generators such as locomotion, simultaneous with intracellular recording. Applying the model to transgenic models of human disorders we explored the hypothesis of an increased level of excitability in a transgenic mouse model of the human motoneurone disease, Amyotrophic lateral sclerosis demonstrating that the increased excitability seen in the neonatal in vitro preparations extends into adulthood. If increased excitability contributes to excitotoxic cell death, why is it not excitotoxic neonatally? We therefore investigated the hypothesis that the axon initial segment may compensate for the early increased excitability and searched for changes in the adult that may counteract this.