In vivo monitoring of evoked noradrenaline release in the rat anteroventral thalamic nucleus by continuous amperometry

• Published in: Journal of neurochemistry 2002-08, Vol.82 (3), p.529-537
• Main Authors: Dugast, C., Cespuglio, R., Suaud‐Chagny, M. F.
• Format: Article
• Language: English
• Subjects: Adrenergic alpha-Agonists - administration & dosage; Adrenergic alpha-Antagonists - administration & dosage; Adrenergic Uptake Inhibitors - administration & dosage; amperometry; Animals; Anterior Thalamic Nuclei - metabolism; Electric Stimulation; electrical stimulation; Electrochemistry; Electrodes, Implanted; evoked release; Extracellular Space - chemistry; Extracellular Space - metabolism; in vivo; Male; Microinjections; Monoamine Oxidase Inhibitors - administration & dosage; noradrenaline overflow; Norepinephrine - analysis; Norepinephrine - metabolism; Rats; Rats, Sprague-Dawley; Serotonin Uptake Inhibitors - administration & dosage; Tetrodotoxin - administration & dosage; Time Factors
• ISSN: 0022-3042; 1471-4159
• DOI: 10.1046/j.1471-4159.2002.00991.x

Continuous amperometry coupled with untreated carbon‐fibre electrodes was used in anaesthetized rats to measure the noradrenaline release evoked in the anteroventral thalamic nucleus by electrical stimulation of the dorsal noradrenergic bundle. As expected, the variations in the oxidation current detected in the anteroventral thalamic nucleus exhibited the characteristics of the in vivo noradrenaline release. They were closely correlated with stimulation and consistent with the anatomy of the noradrenergic system involved. They were abolished by the ejection of tetrodotoxin in the vicinity of the carbon‐fibre electrode, diminished by clonidine, an alpha‐2 agonist, and restored by yohimbine, an alpha‐2 antagonist. Furthermore, the time course of these variations was dramatically increased by desipramine, a specific noradrenaline reuptake blocker. In contrast, neither dopamine nor serotonin reuptake blockers, nor the monoamine oxidase inhibitor pargyline were able to alter them. The main advantage of the present approach is its excellent time resolution. We show here for the first time that after single pulse stimulation, noradrenaline is released and eliminated in 118 milliseconds, this time lapse corresponding to the maximal period beyond which subsequent noradrenaline releases could not add up. These observations are in good agreement with the physiological relationship previously observed between impulse flow and noradrenaline overflow.