Scientists erase and restore memory
The ability to selectively erase, implant, or restore memories has been the focal point of many works of fiction and fantasy. Memory manipulation has been used as both a storytelling device and a crucial plot element in countless works of fiction, from the sci-fi cult hit “Total Recall” to the romance drama “Eternal Sunshine of the Spotless Mind.”
A more recent example would be Spider-Man, who found himself at the center of a mind-altering adventure for more than a year’s worth of publication.
While previous research efforts have indicated that memories can indeed be modified on a genetic level, a recently published study in Nature describes a possible new way to intentionally erase or restore memories through optical stimulation with lasers.
A team of researchers from the University of California, San Diego (UCSD) School of Medicine have succeeded in erasing and restoring memories in genetically-engineered laboratory rats. Their study is said to be the first to lend credence to the theory that the underlying basis for memory is a process known as long-term potentiation (LTP).
This is made possible by stimulating nerves in the brain at frequencies that weaken or strengthen the synapses—the gaps between nerve cells that serve as “bridges” for information to pass through in the form of either a chemical or electrical signal.
Manipulating memories at will
Dr. Roberto Malinow, the senior author of the study, said that applying a stimulus to the brain could either strengthen or weaken synaptic connections. “We can form a memory, erase that memory and we can reactivate it, at will,” explained Dr Malinow, a neuroscience professor at the UCSD.
Studies conducted by researchers in Norway in the 1960s and 1970s have shown that subjecting the neurons within a region of the brain called the hippocampus with repeated electrical signals appeared to enhance these cells’ ability to pass information on to their “neighbors.” This process – called “long-term potentiation” or LTP – had long been suspected to be the prime factor behind learning and memory formation.
After four decades of fruitlessly trying to establish LTP as the basis for memory, Malinow and his team’s research may have effectively demonstrated the role of LTP in memory formation.
“We were playing with memory like a yo-yo,” said Malinow.
Of mice, minds, and lasers
The rats’ brains were genetically modified to produce a light-sensitive protein that is activated with a pulse of blue light. This pulse was delivered to the rats’ brains through an implanted optical fibre.
The researchers then conditioned the rats to associate the stimulation delivered through the optical fibre with pain by sending light pulses to their brains and electric shocks to their feet. This led to the rats reacting with fear each time the optical pulses were activated, and their stimulated nerve synapses displayed chemical changes – an indicator of synaptic strengthening.
Afterwards, a low-frequency series of optical pulses were delivered to the rats’ brains. After a period of time, the rats no longer reacted with fear when subjected to the original frequency of optical stimulation, indicating that they no longer associated pain with the signal. This process, known as long-term depression (LTD), weakened the rats’ synaptic connections.
Most surprisingly, however, was the discovery that the researchers could actually restore the pain-association memory by subjecting the rats’ nerves to a series of optical pulses at a higher frequency. Sure enough, the rats reacted with fear once again when they experienced the original stimulation.
“We can cause an animal to have fear and then not have fear and then to have fear again by stimulating the nerves at frequencies that strengthen or weaken the synapses,” said Sadegh Nabavi, lead author of the study.
Hope for Alzheimer’s
Malinow and his fellow researchers theorize that if the results of this study prove to be applicable to humans, their findings would be of significant help in advancing treatments for patients with Alzheimer’s disease. Malinow believes that this procedure could counteract the weakening of synaptic connections in Alzheimer’s patients due to the accumulation of beta amyloid protein fragments in their brains.
“We have shown that the damaging products that build up in the brains of Alzheimer’s disease patients can weaken synapses in the same way that we weakened synapses to remove a memory,” explained Malinow.
“So this line of research could suggest ways to intervene in the process.”
By : Mikael Angelo Francisco, GMAnetwork.Com