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The K+-induced increases in noradrenaline and dopamine release are accompanied by reductions in the release of their intraneuronal metabolites from the rat anterior hypothalamus
Authors:E. Badoer  H. Würth  D. Türek  F. Qadri  K. Itoi  P. Dominiak  Th. Unger
Affiliation:(1) Department of Pharmacology, University of Heidelberg and German Institute for High Blood Pressure Research, Im Neuenheimer Feld 366, D-6900 Heidelberg, Federal Republic of Germany;(2) Department of Physiology, Ludwig-Maximilians University of Munich, Pettenkoferstrasse 12, D-8000 Munich 2, Federal Republic of Germany
Abstract:Summary The novel technique of microdialysis has been used to examine the basal and K+-induced release of catecholamines and metabolites from the anterior hypothalamus of the urethane-anaesthetized rat in vivo. A high pressure liquid chromatographic assay was developed to simultaneously measure endogenous noradrenaline, dopamine and their intraneuronal metabolites 3,4-dihydroxyphenylglycol (DOPEG) and 3,4-dihydroxyphenylacetic acid (DOPAC) respectively, in each 60 mgrl dialysate sample. The effect of replacing Ca2+ in the perfusion fluid with a low concentration of Cd2+, which blocks Ca2+ effects, was also studied. Increasing the K+ concentration in the perfusion fluid elicited a concentration-dependent increase in noradrenaline and dopamine release. In contrast, there were marked reductions in DOPEG and DOPAC which were not concentration-dependent. In the Ca2+-depleted conditions, the K+-induced increase in amine release was significantly attenuated, but the reductions in the metabolites were not affected. We suggest that the mechanisms contributing to the observed reductions in the metabolites may be inhibition of neuronal reuptake, an increase in neuronal efflux, an enhancement of vesicular uptake and a decrease in vesicular efflux.Send offprint requests to E. Badoer at the above address
Keywords:Brain microdialysis  Anterior hypothalamus  Noradrenaline  Dopamine  3,4-Dihydroxyphenylglycol  3,4-Dihydroxyphenylacetic acid
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