Motor control in mice gained increasing interest during recent years, since a great number of transgenic and mutant mice have been generated with different motor disorders which resemble the symptoms of human diseases as e.g. spasticity, hyperexplexia or amyotrophic lateral sclerosis. While molecular and genetic approaches have revealed valuable findings of the background of these diseases an analysis of the systemic disorders at the motor level is still missing. In order to help bridge the gap between the molecular and the clinical level we investigated the reflex pathways to lumbar extensor motoneurones in fully anaesthetized mice (initial anaesthesia pentobarbital sodium 70 mg/kg i.p., after cannulation of the jugular vein anaesthesia maintained with methohexital sodium 60-70 mg/kg/h as required). Motoneuronal reflex activity was either recorded intracellularly from motoneurones innervating the tibial nerve (Tib, including gastrocnemius soleus, GS, and flexor digitorum longus) or with monosynaptic reflex testing of the GS motoneurone pool. Thresholds are given in relation to the fibres with the lowest threshold. The data were compared with the data known from the cat. With intracellular recording of tibial motoneuones monosynaptic group I EPSPs occurred with a latency from the group I incoming volley of 0.4-0.6 ms (intraindividual SD of less than 0.04 ms). Homonymous or synergistic group II EPSPs (no group II IPSPs were observed) occurred with a threshold of 1.7-2 T, were maximal with 7-10 T and had a latency to the group I incoming volley of around 2.5 ms (with an intraindividual SD of around ± 0.11 ms).The mean difference between the group I and group II incoming volley was 0.41 ms (s.d. ± 0.15 ms), indicating an at least disynaptic transmission from group afferents. Monosynaptic reflexes of the GS were facilitated by conditioning stimulation of the common peroneal nerve (with 5 T) the sural nerve (2 T) and the tibial nerve (5 T), i.e. by a variety of different, probably flexor reflex afferents. This facilitation persisted after high lumbar spinalization. The results revealed latencies and thresholds of group I and II EPSPs in the mouse which are similar to those observed in the cat (Lundberg et al. 1987). However, in contrast to reflex actions in the cat flexor reflex afferents induce predominantly extensor facilitation in the ankle and foot extensors. Possibly, this difference is due to different patterns of the limbs of small mammals during locomotion compared to larger mammals.