NOVEL DISTRIBUTION OF SODIUM-DEPENDENT [H-3] NALOXONE BINDING-SITES IN RAT-BRAIN

Sodium is known to increase opioid antagonist binding (1). Although th e alkylating agent N-ethylmaleimide (NEM) inhibits normal [H-3]naloxon e binding, it has no effect on sodium-dependent [H-3]naloxone binding (2). These studies were performed to determine whether NEM would also selectively reveal sodium-dependent [H-3]naloxone binding sites in tis sue sections and whether sodium-dependent sites have the same anatomic al distribution as normal [H-3]naloxone binding sites. Displacement bi nding assays showed that sodium-dependent [H-3]naloxone binding sites were low affinity mu sites uncoupled from G proteins. Autoradiographic studies showed that the anatomical distribution of sodium-dependent [ H-3]naloxone binding was distinct from that of normal [H-3]naloxone bi nding, with the highest levels in the bed nucleus of the stria termina lis, lateral hypothalamus, lateral amygdala, median raphe nucleus and parabrachial nucleus.