Scientists erased and then restored memories in genetically engineered rats using a flash of light.
The study provides the first evidence of a cause-and-effect relationship between neurons and memories, an NIH/National Institute of Mental Health news release reported.
"Our results add to mounting evidence that the brain represents a memory by forming assemblies of neurons with strengthened connections, or synapses," Roberto Malinow, M.D., Ph.D., of the University of California, San Diego (UCSD), a grantee of the NIH's National Institute of Mental Health (NIMH), said in the news release. "Further, the findings suggest that weakening synapses likely disassembles neuronal assemblies to inactivate a memory."
"Beyond potential applications in disorders of memory deficiency, such as dementia, this improved understanding of how memory works may hold clues to taking control of runaway emotional memories in mental illnesses, such as post-traumatic stress disorder," NIMH director Thomas R. Insel, M.D said in the news release.
The researchers suspected that connections between neurons called long-term potentiation (LTP) were the key to memory formation. The team made their findings by modifying the strength of synapses in memory circuits; they did this using optogenetics, which controls brain activity with a laser.
The researchers used electrical shocks so that the rats would associate pain with a specific tone. If the memory is present the rats would freeze and show less reward-seeking behaviors when the tone was played. The team paired the shock with optogenetic stimulation instead, which stimulated neurons in the fear memory circuit.
"It's just a jungle in the brain - too many nerve cells coming through in any one place," Malinow said.
The team was able to strengthen or weaken the connections between neurons in the circuit allowing for a process called long-term depression (LTD). This allowed them to create a fear memory, remove it, and then restore it.
"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," Malinow said. "So this line of research could suggest ways to intervene in the process."
"In addition to eliminating any doubt about a link between LTP/LTD with memories, this work highlights the staggering potential of precision targeting and circuit manipulation for alleviating maladaptive memories," project officer Chiiko Asanuma,Ph.D., of the NIMH Division of Neuroscience and Basic Behavioral Science, said in the news release.
