Noradrenaline action on electrical activity of cultured trigeminal ganglion neurons (TGN) was studied. Noradrenaline (NA) application on an isolated sensory neuron simulates sympathetic-sensory influences on signal transmission via primary trigeminal afferents. In response to depolarization the neurons exhibited three types of activity: tonic (68%, n = 52), adaptive (28%, n=21) and delayed-generation (4%, n=3). Under the NA application, part of tonic neurons (25%, n=13) lost the tonic firing ability; also, reducing of action potential (AP) (from 93±5 mV to 68±4 mV) and afterhyperpolarization (from -28±2 mV to -22±2 mV) amplitude was observed. In 46% (n=24) of tonic neurons, AP amplitude (from 98±2 mV до 86±3 mV) and repolarization phase duration (from 3.2±0.2 ms to 2.6±0.2 ms) were decreased. In adaptive and delayedgeneration neurons, the NA application led to a reducing in AP amplitude (from 91±1mV to 76 ±2 mV; n=17) and repolarization phase duration (from 4.2±0.5 ms до 3.2±0.3 ms; n=17). When hyperpolarized, tonic and adaptive neurons demonstrated inward rectification; this effect was reduced under the influence of NA (the relative inward rectification coefficient values compared to control were 0.84 ± 0.1 and 0.76 ± 0.04 respectively). The data obtained suggests that adrenergic action on electrical activity of TGN is provided via adrenergic receptors influence on high-threshold voltage-gated calcium channels and hyperpolarization-activated channels.