Noradrenaline inhibits glutamate release in the rat bed nucleus of the stria terminalis: In vivo microdialysis studies

The microdialysis technique was used to simultaneously study the in vivo ex tracellular levels of noradrenaline, glutamate, and gamma aminobutyric acid (GABA) in the bed nucleus of the stria terminalis in order to assess the r egulation that noradrenaline may exert upon the release of amino acid neuro transmitters. Perfusion through the probe with UK14304, a selective alpha(2 )-adrenergic agonist, produced a significant decrease of noradrenaline and glutamate extracellular levels. Perfusion through the probe with RX821002, a selective alpha(2)-adrenergic antagonist, produced a significant increase of noradrenaline and glutamate basal extracellular levels. Perfusion with prazosine, a selective alpha(1)-adrenergic antagonist, produced a significa nt decrease of noradrenaline basal extracellular levels without affecting g lutamate levels. Under the same conditions, GABA basal extracellular levels were not changed in the presence of any of the alpha-adrenergic ligands st udied. The perfusion of high potassium through the probe induced a signific ant Ca++- dependent release of the three neurotransmitters; however, extrac ellular noradrenaline returned to normal levels even though potassium was s till present. In addition, it was observed that alpha-adrenergic receptor l igands exerted differential effects upon K+-induced release of noradrenalin e and glutamate. Perfusion with the nonselective alpha-adrenergic antagonis t, phenoxybenzamine, presented a biphasic effect upon K+-induced release of noradrenaline; a significant decrease during the first 5 min of stimulatio n followed by a significant increase in the next 5 min of stimulation. Perf usion with RX821002 produced a significant increase in K+-induced release o f noradrenaline that returned to normal basal values before the end of the stimulation period. In contrast, local perfusion with prazosine caused a si gnificant decrease of K+-induced noradrenaline release. In the case of glut amate, perfusion through the probe with phenoxybenzamine produced a signifi cant increase in K+-induced release of glutamate. In addition, RX821002 and prazosine produced a significant increase in K+-induced release of glutama te. Perfusion through the probe with UK14304 produced a significant decreas e of both noradrenaline and glutamate K+-induced release. The present resul ts show that noradrenaline in the bed nucleus of stria terminalis exerts a significant inhibition over its own release through alpha(2)-adrenergic rec eptors and over glutamate release mainly through alpha(2)-adrenergic recept ors. Thus, the results suggest that noradrenaline in the bed nucleus of the stria terminalis maintains an inhibitory tone over the information flow me diated by glutamate. J. Neurosci. Res. 55:311-320, 1999. (C) 1999 Wiley-Lis s, Inc.