The Formation of False Memories in the Brain
By: Sai Srihaas Potu
Memories are complex. While you might imagine memory as a black or white element, the truth is memories are subject to change, malleable, and often unreliable. Events are moved from your brain’s temporary memory to permanent storage while you sleep. The transition, however, isn’t absolute. Elements of the memory may be lost. This is where false memories can begin.
A false memory is a recollection that seems real in your mind but is fabricated in part or whole. Most false memories aren’t malicious or even intentionally harmful. They’re shifts or reconstructions of memory that don’t align with the true events. The phenomenon of false memory has been well-documented. In many court cases, defendants have been found guilty based on testimony from witnesses and victims who were sure of their recollections, but DNA evidence later overturned the conviction.
In a step toward understanding how these faulty memories arise, MIT neuroscientists have shown that they can plant false memories in the brains of mice. They also found that many of the neurological traces of these memories are identical to those of authentic memories. Their study also provides further evidence that memories are stored in networks of neurons that form memory traces for each experience we have.
Neuroscientists have long sought the location of these memory traces, also called engrams. In the pair of studies, Tonegawa and colleagues at MIT’s Picower Institute for Learning and Memory showed that they could identify the cells that makeup part of an engram for a specific memory and reactivate it using a technology called optogenetics.
Episodic memories, memories of experiences, are made of associations of several elements, including objects, space, and time. These associations are encoded by chemical and physical changes in neurons, as well as by modifications to the connections between the neurons. Where these engrams reside in the brain has been a longstanding question in neuroscience.
In the 1940s, Canadian neurosurgeon Wilder Penfield suggested that episodic memories are located in the brain’s temporal lobe. When Penfield electrically stimulated cells in the temporal lobes of patients who were about to undergo surgery to treat epileptic seizures, the patients reported that specific memories popped into mind. Later studies of the amnesiac patient known as H.M. confirmed that the temporal lobe, including the area known as the hippocampus, is critical for forming episodic memories.
However, these studies did not prove that engrams are stored in the hippocampus. To make that case, scientists needed to show that activating specific groups of hippocampal cells is sufficient to produce and recall memories. To achieve that, Tonegawa’s lab turned to optogenetics, a new technology that allows cells to be selectively turned on or off using light.
For this pair of studies, the researchers engineered mouse hippocampal cells to express the gene for channelrhodopsin, a protein that activates neurons when stimulated by light. They also modified the gene so that channelrhodopsin would be produced whenever the c-fos gene, necessary for memory formation, was turned on.
In the first study, the researchers conditioned these mice to fear a particular chamber by delivering a mild electric shock. As this memory was formed, the c-fos gene was turned on, along with the engineered channelrhodopsin gene. This way, cells encoding the memory trace were labeled with light-sensitive proteins.
The next day, when the mice were put in a different chamber they had never seen before, they behaved normally. However, when the researchers delivered a pulse of light to the hippocampus, stimulating the memory cells labeled with channelrhodopsin, the mice froze in fear as the previous day’s memory was reactivated. In their next study, the researchers explored whether they could use these reactivated engrams to plant false memories in the mice’s brains.
First, the researchers placed the mice in a novel chamber, A, but did not deliver any shocks. As the mice explored this chamber, their memory cells were labeled with channelrhodopsin. The next day, the mice were placed in a second, very different chamber, B. After a while, the mice were given a mild foot shock. At the same instant, the researchers used light to activate the cells encoding the memory of chamber A.
On the third day, the mice were placed back into chamber A, where they now froze in fear, even though they had never been shocked there. A false memory had been incepted: The mice feared the memory of chamber A because when the shock was given in chamber B, they were reliving the memory of being in chamber A.
Moreover, that false memory appeared to compete with a genuine memory of chamber B, the researchers found. These mice also froze when placed in chamber B, but not as much as mice that had received a shock in chamber B without having the chamber A memory activated. The researchers then showed that immediately after the recall of the false memory, levels of neural activity were also elevated in the amygdala, a fear center in the brain that receives memory information from the hippocampus, just as they are when the mice recall a genuine memory.
False memories aren’t rare. False memories can happen to anyone. Some people may be more likely to experience them. The good news is that most false memories are harmless and may even produce some laughs when your story conflicts with someone else’s memory of it. However, scientists must continue to conduct research in this field in order to understand the mechanisms that control the onset of false memories as this is an important symptom in many mental health disorders.
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