Excitability and conduction of nerve fibres in mice gained increasing interest, since transgenic mice have been generated with alterations of nerve and myelin properties, partly resembling the clinic of human diseases. The conduction velocity by itself may not be the crucially changed parameter, e.g. if there are metabolic deficits of the myelin function. Therefore, we now investigated the excitability and conduction of central nerve fibres in mice with metabolic myelin-axon deficits. The Experiments were performed in fully anaesthetised mice (initially pentobarbital sodium 70 mg/kg i.p., continuance with methohexital sodium 60-70 mg/kg/h i.v.). A tracheotomy was performed for artificial ventilation after paralysation (paralysation with pancuronium bromide 800 μg/kg/h intraperitoneally, artificial ventilation with a gas mixture of O2 (47.5%), CO2 (2.5%), and N2 (50%) at about 120 strokes/min).. ECG, heart rate, core body temperature and blood O2 saturation were permanently monitored and used to control the anaesthetic state. The lumbar spinal cord and dorsal roots were exposed by a laminectomy. Stimulation was performed at the dorsal root L4 with 100 Hz and a sub-maximal stimulus strength for 10 min. Recovery was tested with 0.1 Hz. The induced compound action potential (CAP) was recorded 7 to 10 mm cranially to the stimulation electrode at the dorsal column (fasciculus gracilis) of the spinal cord. The results from wild type mice were compared with results from two different types of transgenic mice: 1.) a model of metabolic support deficit in conditional NR1-KO mice (lacking NMDA-receptors in oligodendrocytes); 2.) a model of a classical neurodegenerative disease ALS, SOD1G93A mice (a deficit of oligodendroglial support of axons has been shown in a similar model of ALS, Lee et al. 2012). In both types of models, the decrement during the high-frequency stimulation period was significantly more pronounced in the transgenic mice compared to wild-type littermates. Time course of recovery was correspondingly delayed in the transgenic mice. The results suggest a deficit of the axon-glial metabolism with regard to energy support from oligodendroglia towards axons during tetanic high frequency stimulation.The experimental approach is of interest for the functional characterisation of nerve fibres with metabolic deficits with or without structural abnormalities, also in classical models of neurodegenerative diseases.