Beta-endorphin causes retrograde amnesia and is released from the rat brain by various forms of training and stimulation.
The endogenous opiate peptide, beta-endorphin (0.4, 1.0, 2.0, and 10.0 microgram/kg) was injected IP into rats immediately after training in a shuttle avoidance task, and its effect on memory retention was evaluated in test sessions carried out 24 h later. The drug was found to cause retrograde amnesia, the ED50 being 1.0 microgram/kg. Beta-endorphin immunoreactivity was measured in the hypothalamus and rest of the brain of rats submitted to training, or test sessions of shuttle avoidance learning, pseudoconditioning in the shuttle-box, tones alone, or foot-shocks alone. After training in any of the four paradigms, there was a marked (46-60%) depletion of beta-endorphin immunoreactivity in the rest of the brain. No changes were detected in the hypothalamus or after test sessions. The loss of beta-endorphin immunoreactivity may be attributed to release of this substance caused by the stimuli used for training. From the present findings, as well as previous observations on the memory-facilitating influence of the opiate receptor antagonist, naloxone, it is concluded that there is a physiological amnesic mechanism mediated by beta-endorphin (and perhaps other opoid peptides as well), which is triggered by the non-associative factors present in the various forms of learning.
D000647:Amnesia / Q000139:chemically induced*; D000648:Amnesia, Retrograde / Q000139:chemically induced*; D000818:Animals; D001362:Avoidance Learning / Q000502:physiology; D001921:Brain / Q000378:metabolism* / Q000502:physiology; D003216:Conditioning, Operant / Q000502:physiology; D004558:Electric Stimulation; D004723:Endorphins / Q000378:metabolism / Q000494:pharmacology* / Q000502:physiology; D005260:Female; D006801:Humans; D007031:Hypothalamus / Q000378:metabolism; D007858:Learning / Q000502:physiology*; D051381:Rats; D001615:beta-Endorphin
D004723:Endorphins; D001615:beta-Endorphin