In vivo voltammetric monitoring of noradrenaline release and catecholamine metabolism in the hypothalamic paraventricular nucleus

The paraventricular hypothalamic nucleus receives a dense noradrenergic innervation. Electrochemically treated carbon fibre electrodes were implanted in the paraventricular nucleus of anaesthetized rats and their locations were histologically controlled after each experiment. Differential normal pulse voltammograms showed an oxidation peak at +50 mV. This peak was mainly due to 3,4-dihydroxyphenylacetic acid synthesized by noradrenergic terminals since: (1) it appeared at the same oxidation potential as 3,4-dihydroxyphenylacetic acid in vitro ; (2) it was rapidly suppressed after inhibition of tyrosine hydroxylase byalpha-methyl- p -tyrosine or monoamine oxidase by pargyline; (3) blockade of dopamine-β-hydroxylase by FLA 63 induced a marked increase in this signal, whereas this drug was without effect in dopaminergic terminals fields (striatum, zona incerta); (4) stimulation of alpha 2 noradrenergic receptors by clonidine (50μg/kg) decreased the peak height and this effect was reversed by piperoxane (30 mg/kg). This oxidation peak corresponded to a 3,4-dihydroxyphenylacetic acid concentration of 2 μM. On the other hand, when recorded from rats which were treated with pargyline 3 h before recording, a small peak appeared at +100 mV. This signal was attributed to the oxidation of extracellular noradrenaline on the basis of the following arguments: (1) it appeared at the same potential as noradrenaline in vitro ; (2) desipramine (25 mg/kg) induced a 4-fold increase in this peak height; (3) piperoxan (2 mg/kg) enhanced this signal and reversed the decrease induced by clonidine (50 μ/Kg); (4) electrical stimulations (bipolar electrode, square pulses, 0.3 ms, 200 μA, 15 Hz for 40 s) in the rostral part of the Al group were followed by an immediate, short-lasting 4-fold increase in the signal.