In previous studies we verified that the synaptic transmission in the nucleus tractus solitarius (NTS) neurons is affected by chronic intermittent hypoxia. Here we evaluated the effect of short-term sustained hypoxia (SH, 24 hours – 10% O2) on the intrinsic properties and synaptic transmission of NTS neurons in the brainstem slices from young rats (3 weeks old) using whole cell patch clamp technique. SH produced no change in resting membrane potential [control: -78.7 ± 2.4 mV (n=15), SH: -72.3 ± 3.7 mV, (n=15)], input resistance [control: 1.4 ± 0.4 GOhm (n=8), SH: 1.4 ± 0.4 GOhm, (n=9)] and capacitance of NTS neurons [control: 14.2 ± 0.9 pF (n=17), SH: 12.4 ± 0.8 pF (n=15)]. However, SH increased the frequency of spontaneous excitatory post-synaptic currents [(sEPSCs) control: 3.6 ± 0.4 Hz (n=18), SH: 7 ± 1.5 pF, (n=15), p<0.05] and the amplitude of evoked excitatory post-synaptic currents [(eEPSCs) control: -289 ± 51 pA (n=15), SH: -472 ± 64 pA (n=15), p<0.05]. Moreover, SH also increased the depression of evoked excitatory post-synaptic currents after five stimuli on afferent fibers in the tractus solitarius [amplitude of 5 evoked currents of control group: 100%, 44%, 34%, 32% and 28% (n=15), amplitude of 5 evoked currents of SH group: 100%, 40%, 28%, 22% and 17% (n=15) *p<0,001 – Two way ANOVA]. These findings suggest that SH affect the excitatory transmission in NTS neurons increasing the release probability in the pre-synaptic terminal. We conclude that 24 hours of SH enhances spontaneous and evoked excitatory synaptic transmission on NTS neurons but does not change their intrinsic properties. These alterations in the synaptic transmission in the NTS neurons induced by SH may play a critical role in the cardiovascular and respiratory problems observed in high altitude.