The hypothalamic paraventricular nucleus is densely innervated by noradrenergic terminals mainly originating in the A1 group within the ventrolateral medulla. An oxidation signal corresponding to extracellular catechols was recorded from the paraventricular nucleus of urethane anaesthetized rats every 1 s by differential pulse amperometry at + 105 mV combined with carbon fiber electrodes. In basal conditions, both extracellular noradrenaline and DOPAC, which are synthesized by noradrenergic terminals, contributed to this oxidation signal. Electrical stimulations of the rostral part of the A1 group were applied for 10 or 20 s every 10 min at physiological frequency (3-20 Hz). They induced an immediate increase in the oxidation signal which lasted as long as the stimulation. This increase was due to the evoked noradrenaline release since it was enhanced by pargyline, desipramine and amphetamine and it was attenuated by alpha-methyl-p-tyrosine and reserpine. The amplitude of the evoked noradrenaline release depended non-linearly on the frequency of the stimulation (from 3 to 20 Hz). When expressed per pulse, noradrenaline release was facilitated four-fold as the frequency increased from 3 to 20 Hz. Central noradrenergic neurons exhibit a tonic activity in a single spike discharge pattern with a mean frequency below 5 Hz but they respond to physiological stimuli by short bursts of action potentials at 20 Hz. Therefore, the present data show that noradrenergic terminals convert physiological impulse flow into noradrenaline release as a high pass filter which enhances the signal-to-noise ratio in response to phasic stimuli.