th the neurotransmitter dopamine, which is associated with pleasurable and painful stimuli. If a blocker for the dopamine receptor was injected into the hypothalamus of the brain 12 hours after the shock -- but not immediately after the shock or nine hours later -- the rats effectively forgot about the experience: seven and 14 days after the shock, they exhibited little to no latency. Conversely, if a dopamine receptor activator was injected 12 hours following a weak shock, the rats remembered the experience as if they had received a strong shock.
In other words, at a specific point following the shock, the researchers could pharmacologically alter these animals' brains, causing them either to forget the traumatic experience, or to remember it more strongly.
The implication, said Roy Wise, chief of the behavioral neuroscience branch in the Intramural Research Program at the National Institute on Drug Abuse, is that "the memories we thought were solid and accurate are not."
The effect depended on the activity of a specific brain protein called BDNF, and on interaction of the hypothalamus with another brain region called the ventral-tegmental area.
"I think it's a really exciting study," said Philip Corlett, of the University of Cambridge and Yale University. "Understanding more about how long-term memories are formed may have huge implications for psychiatric diseases, which often are diseases of memory."
Assuming the results can be replicated in humans -- which is by no means certain, given that the rats were treated via shunts in the brain, a delivery method unlikely to be used in humans -- potential applications run the gamut from boosting learning to ameliorating the effects of psychiatric diseases. But perhaps the most obvious human application involves post-traumatic stress disorder (PTSD).
"If you could get to somebody soon after the traumatic experience, you might be able to interfere with this conso
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