It may be possible to develop drugs to delete memories that trigger anxiety and post-traumatic stress disorder (PTSD) without affecting other important memories of past events, a new study suggests.
Different types of memories stored in the same neuron of the marine snail Aplysia can be selectively erased, according to the study by Columbia University Medical Center and McGill University and published in Current Biology.
During emotional or traumatic events, multiple memories can become encoded, including memories of any incidental information that is present when the event occurs. In the case of a traumatic experience, the incidental, or neutral, information can trigger anxiety attacks long after the event has occurred, the researchers said.
“The example I like to give is, if you are walking in a high-crime area and you take a shortcut through a dark alley and get mugged, and then you happen to see a mailbox nearby, you might get really nervous when you want to mail something later on,” said Samuel Schache of Columbia, a coauthor of the study.
In the example, fear of dark alleys is an associative memory that provides important information based on a previous experience. Fear of mailboxes, however, is an incidental, non-associative memory that is not directly related to the traumatic event.
“One focus of our current research is to develop strategies to eliminate problematic non-associative memories that may become stamped on the brain during a traumatic experience without harming associative memories, which can help people make informed decisions in the future — like not taking shortcuts through dark alleys in high-crime areas,” Schacher said.
Previous research suggested that increases in synaptic strength in creating associative and non-associative memories share common properties. Selectively eliminating non-associative synaptic memories would be impossible, because for any one neuron, a single mechanism would be responsible for maintaining all forms of synaptic memories, the previous research suggested.
The new study tested that hypothesis by stimulating two sensory neurons connected to a single motor neuron of the marine snail Aplysia. One sensory neuron was stimulated to induce an associative memory and the other to induce a non-associative memory.
By measuring the strength of each connection, the researchers found that the increase in the strength of each connection produced by the different stimuli was maintained by a different form of a Protein Kinase M (PKM) molecule (PKM Apl III for associative synaptic memory and PKM Apl I for non-associative). They found that each memory could be erased – without affecting the other — by blocking one of the PKM molecules.
“Our study is a ‘proof of principle’ that presents an opportunity for developing strategies and perhaps therapies to address anxiety,” said Schacher.
Future studies in preclinical models are needed to better understand how PKMs are produced and localized at the synapse before researchers can determine which drugs may weaken non-associative memories, the authors said.