Disruption of trophic communication between the motoneurons and their target muscle fibres by axon injury increases excitability of motoneurons and alters the recruitment order of motor units. These alterations are concomitant with the de novo expression of the neuronal isoform of nitric oxide synthase (NOS-I) which synthesizes the free radical gas nitric oxide (NO). NO is a modulator in certain neurotransmitter systems and recently it has been demonstrated to play a key role in the synaptic remodelling induced in hypoglossal motoneurons (HMNs) by XIIth nerve injury (1). The aim of this work was to determine the role of NO on intrinsic membrane properties and synaptic inputs to the HMN pool. To this end, we studied the effect of acute application of NO donor diethylamine NOnoate (DEA/NO, 10μM) on HMNs. Hypoglossal nuclei-containing brainstem slices were prepared from terminally anaesthetised female Wistar rats (P7, 250-300 μm). Antidromically identified HMNs were recorded in the whole-cell patch clamp mode following the procedures previously established in this laboratory (2). Monosynaptic excitatory postsynaptic potentials (EPSPs) were triggered in HMNs by electrical stimulation within the ventrolateral reticular formation (VRF). On average, 44 neurones included in this study had membrane potential (Vm) =-53.7 ± 0.6 mV (mean ± S.E.M.), membrane resistance (Rm) = 67.6 ± 3.8 Mohm, threshold current required to trigger an action potential generation, rheobase (Rh) = 0.27 ± 0.035 nA. 20 of 30 HMN tested responded to the stimulation of VRF. A 10 min application of NO donor DEA/NO resulted in a slight but significant depolarisation of the membrane of HMN (7.6 ± 0.9% of control, p < 0.001, n = 25, Student's paired t test). Rh decreased after DEA/NO administration by 20.4 ± 7.4% (p 0.05). Interestingly, monosynaptic EPSPs were not altered by NO administration (0.53±1.75% of control, n= 11). These findings suggest that NO can induce changes in intrinsic membrane properties of HMN and that similar effects might occur in response to axonal injury.