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We Use Just 20 % of Our Brains to Make MemoriesDifferent memories, different neurons |
By Stefan Anitei, Science Editor
20th of April 2007, 13:46 GMT
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You may hear continuously that you do not use your brain enough.
For some it can be obvious: they use a neuron to eat, one to have sex, one to s**t and one to piss.
But on a scientific level, a new research found that we really could be using just 20 % of the neurons in our midbrain to form memories.
Researchers at the University of California, Los Angeles, and The Hospital for Sick Children in Toronto investigated neurons in the mice brain's amygdalae (two almond-shaped nuclei on the lateral midbrain linked with learning and memory) to assess CREB (Camp response element binding) protein's role in triggering neurons to make memories.
CREB raises the proteins synthesis in cells and is linked to memory formation in species from sea slugs to humans.
The team injected a compound meant to return CREB synthesis to normal in mice that had been engineered to produce lower levels.
These memory-impaired mice could perform as well as normal mice in memory tests after receiving the shot.
The investigators played a sound and then shocked the mice; when the sound was played again, normal mice and those with rescued CREB function displayed a typical fear reaction.
When they dissected the mice's brains, the fluorescent probes attached to the CREB vectors showed that they had affected just 20 % of the amygdala neurons.
"We thought that we would have to affect a lot more neurons in order to see a big change in memory," said co-author Sheena Josselyn, a neurophysiologist at The Hospital for Sick Children.
"Not all [neurons] participate in every memory. Maybe we're biasing these neurons to participate in this memory and [CREB is] all you need to compel it."
To see if the CREB-producing cells were involved, the team inserted a probe giving off a fluorescent tag from the RNA of the Arc gene, with risen activity when neurons are active.
The RNA synthesized in the nucleus is transported to dendrites, the neuron projection that collects information from other cells.
"Arc RNA provides a really good molecular marker of when this neuron was active," said Josselyn.
"If the team found RNA in the nucleus of neurons immediately after a training event, they knew cells had been active within the last five minutes; if the probe was in the dendrite, they estimated activity had taken place 20 minutes earlier."
CREB-enabled nuclei were three times more likely to present the Arc signature inside, than neuronal nuclei in CREB-impaired individuals.
Normal mice injected with a vector that would selectively decrease CREB function in some of their neurons could learn normally, thus the healthy neurons were still making enough CREB to produce the memories.
The memory trace, betrayed by Arc, revealed that just 20 % of neurons were activated.
"We think that it's really a competition, that neurons are really battling it out amongst each other to be involved in the memory-making process. It's like grading on a curve … the same number (20 %) of students are going to get As"-or in this case help make the memory" said Josselyn.
So, each memory is formed by 20 % of the neurons, but not the same ones each time.
By boosting CREB function, brain memory ability could be improved.
"The brain likely differentiates different memories by having different neurons encode them. In the future, this mechanism could be harnessed to produce a new treatment for Alzheimer's disease. In time, we're going to have some sort of neuron-replacement therapy for Alzheimer's," she said.
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