Abstract

The bed nucleus of stria terminalis (BNST) contains the highest concentration of noradrenaline (NA) in the brain. Minislices of the ventral portion of the bed nucleus of stria terminalis (vBNST) were used to study the release of endogenous NA. High K+ induced a Ca2+-dependent and reserpine-sensitive release of NA. Clonidine (1 mu M), an alpha(2)-noradrenergic receptor agonist, significantly decreased K+-induced release of NA, whereas yohimbine (1 mu M), an alpha(2)-noradrenergic antagonist, increased this release. N-Methyl-D-aspartate (NMDA), a specific agonist of NMDA-type glutamate receptors. evoked the release of NA from vBNST minislices. In the presence of D-serine (10 mu M), an agonist at the glycine site associated with the NMDA receptor, the NMDA effect was significantly higher. Glycine (1 mu M) also increased NA release evoked by NMDA. However, glycine exhibited a significant effect by itself, suggesting the existence of strychnine-sensitive glycine receptors in vBNST. Endogenous NA release induced by 40 mM K+ and NMDA was not additive. Thus, vBNST minislices seem to be a good model to study the release of endogenous NA in the CNS. Such NA release in the vBNST is regulated by alpha(2)-noradrenergic receptors and by glutamate through NMDA receptors.