The role of an endogenous amnesic mechanism mediated by brain beta-endorphin in memory modulation

1. Post-training administration of the opiate receptor antagonist naloxone facilitates the memory consolidation of a wide variety of tasks by rats. 2. Post-training administration of subanalgesic doses of beta-endorphin causes retrograde amnesia. This effect is shared by other opiates and opioids and is competitively antagonized by naloxone. These other opiates and opioids probably act by the release of endogenous beta-endorphin. 3. During various forms of aversive and non-aversive training beta-endorphin (but not Met-enkephalin) is released in the rat brain in amounts compatible with amnestic doses of this substance. 4. A number of treatments that cause naloxone-reversible retrograde amnesia, i.e. high doses of ACTH or adrenaline, low doses of morphine or of opioids, electroconvulsive shock, release massive amounts of beta-endorphin and Met-enkephalin in the rat brain. 5. These findings point to the existence of a physiological amnesic mechanism mediated by beta-endorphin, and perhaps other opioids as well, that normally prevents memory from being as good as it could be, and when operating at an exaggerated level may cause complete amnesia. 6. This mechanism interacts with other systems that influence memory consolidation (central dopaminergic and noradrenergic pathways, ACTH, peripheral adrenaline) and is a powerful modulator of their activity. 7. One possible role of the amnesic mechanism during training is to cause the rapid forgetting of adventitious learning that may interfere with acquisition of the main tasks for which animals are being trained. 8. Either through this action, or by some direct effect, beta-endorphin facilitates retrieval of a variety of behaviors in the rat when given before a test session.