Norepinephrine (NE) is the neurotransmitter of the sympathetic branch of the autonomous nervous system in charge of fight and flight responses at physiological and behavioral level. NE-receptors are expressed in different organs of the body including many brain regions and peripheral nervous system. Olfactory sensory neurons (OSNs) express NE-receptors, and NE application to OSNs modulates action potential firing. Vomeronasal organ (VNO) makes part of the mouse accessory olfactory system and its main function is to detect pheromones and regulate social behaviors of the animal. While the effect of NE on the OSN has been studied, the effect of NE on the accessory olfactory systems remains unknow. Here we investigated whether NE directly affects the electrical properties of mouse vomeronasal sensory neurons (VSN) from acute slices, using the patch clamp technique in whole cell mode. We found that in VSNs (n = 10; *p< 0.05, t-test), NE (50 µM) application increases spiking frequency in response to current injection steps. To explain this effect on VNO neurons, one the candidates is the AP machinery, that’s because the experiments were performed in absence of transduction cascade activation, underlying an independent mechanism, which is downstream of it. To test the current involved in the AP, were used voltage clamp recording, the first candidate is the voltage-activated sodium channels, we isolate sodium current using an internal solution contained 140 mM CsCl a typical impermeable cation by voltage-activated potassium channels and the application in the extracellular bath of 100 µM of CdCl2 to block calcium conductance, we found that NE modulates voltage-activated sodium channel activation in VSNs shifting the activation curve to negative potentials ( 8.65 mV ± 2.3 mV ,n=6-9 ,**p<0.01).