For Release February 12, 1998
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Study Yields New Model of Memory Retention: Neurotransmitter Blocks Synaptic Weakening
Waltham, Mass. -- Neuroscientists at Brandeis University have found new evidence of how memory is selectively retained by the brain. In a paper published in the Feb. 15 Journal of Neuroscience, John Lisman, Ph.D., and Nonna Otmakhova, Ph.D., show how the chemical dopamine operates in the hippocampus of the brain to retain memories. Dopamine appears "to modify the rules of activity-dependent synaptic plasticity," the authors say. The major new finding is that the weakening of synapses, the connection between nerve cells (neurons), is blocked by dopamine. That weakening is thought to be responsible for a loss of memory -- in other words, forgetting.
Lisman, professor of biology and Volen National Center for Complex Systems at Brandeis, has long studied the neuroscience of memory, especially synaptic plasticity ñ the changes in the brain that occur in response to particular stimuli and which are thought to encode memory. There are two kinds of brain processes by which synapses are modified to create learning and memory, he explains: long-term potentiation (LTP), which makes synapses stronger, and long-term depression (LTD), which makes synapses weaker.
"Many changes in behavior and memory are related to changes in the strength of synapses in the brain," he says. "What are the rules governing these changes? That's where long-term potentiation and long-term depression come in."
Lisman and Otmakhova, a postdoctoral fellow, studied how the neurotransmitter dopamine activates certain receptors in the hippocampus. Dopamine is released when the organism receives positive feedback or a "reward" (e.g., food). Their results show that dopamine seems to operate as a chemical "reward" for learning on a cellular level by blocking the erasure of memories.
In a prior study, they found that dopamine administered after the induction of a stimulus had no reinforcing effect on long-term potentiation, the synaptic activity equated with memory. That was disappointing, Lisman says, since dopamine is likely to be released after a stimulus. In the new study, they went one step farther, extending their study to the process of synaptic weakening, or LTD, that occurs after the initial signal. They found that administering dopamine to these neurons strongly blocked the weakening process, and helped sustain higher synaptic strength. The data point to a new model for selectively remembering information that is followed by reward.
Based on the new results, Lisman suggests that all information is initially encoded by the synapse, but automatically "erased" by a synaptic weakening process (depotentiation), most likely during a vulnerable window period of 5 to 10 minutes after the initial signal. But if dopamine is provided during this window, it blocks depotentiation and the signal is retained, with long-term potentiation of the synapse resulting in "memory." Dopamine appears to block depotentiation through other chemical intermediaries. The authors say this model could serve to explain phenomena like individuals with "photographic memory," who can recall nearly all incoming information ñ perhaps through a failure of the normal "erasure" mechanism.
The study sheds light on how the brain selectively retains memories about events that turn out well. "We've found a building block of the system that leads to selective retention of actions that result in a reward," says Lisman. The study does not look at how aversion ñ things that have a "bad outcome," like receiving a pain signal or loud noise ñ affects learning. Dopamine is implicated in some conditions affecting behavior, including schizophrenia and attention deficit disorder.
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