Postsynaptic inhibitory actions of catecholamines and opioid peptides in the bed nucleus of the stria terminalis.

Effects of catecholamines, enkephalins and related compounds on electrical activity of the bed nucleus of stria terminalis (BST) were studied in vitro on thin BST sections prepared from guinea pig brains. Norepinephrine (NE) and epinephrine (E) suppressed field potentials elicited by a single shock to the stria terminalis (ST). The effects of NE and E were mimicked by phenylephrine and blocked by phenoxybenzamine. Isoproterenol and dichloroisoproterenol were without effect. NE and E suppressed the spontaneous firing of BST neurons and discharges elicited by ST stimulation. Dopamine was a less potent depressant. [D-Ala2]-Met-enkephalinamide (EKA) suppressed the field potentials and spike discharges elicited by ST stimulation. Spikes occurring spontaneously or during administration of glutamate were also suppressed by EKA. The action of EKA was blocked by naloxone. Late inhibition induced by stimulation of the lateral division of the ST was blocked by naloxone in about a third of the neurons examined. These results indicate that norepinephrine suppresses the activity of BST neurons by activating postsynaptic alpha-receptors. It is also suggested that opioid peptides mediate inhibitory control of the amygdala over the BST.