Researchers have recently discovered two different types of memory use completely different processes in the same nerves, opening the way for a new pharmaceutical solution for treating anxiety and post-traumatic stress disorder (PTSD).
The find challenges earlier research that had suggested memories of traumatic events used the same nerves in the same ways, making them impossible to physically distinguish.
A team of scientists from Columbia University Medical Center (CUMC) and McGill University analysed neurons from a marine snail called an Aplysia in order to test a hypothesis explaining why memories of incidents surrounding a bad experience can themselves trigger anxiety.
Neurons build long term memories by reinforcing the chemical bridges called synapses that link them together.
An experience that could harm an organism, such as touching a hot surface or experiencing violence, becomes encoded as an associative memory as the connections between neurons strengthens.
Experiences aren't always quite so cut-and-dried; an organism might touch a hot surface as it hears a bell, or hear a dog bark nearby as they are assaulted. The bell might be related, or might just be incidental – neurons still record the information in case it's necessary.
Sometimes this incidental memory doesn't do the individual any favours, triggering anxieties that do little to help prevent them from future harm.
Many people with PTSD re-experience trauma by association with seemingly unrelated stimuli.
"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," says researcher Samuel Schacher from CUMC.
Anxiety caused by the incidental memory of the mail-box can interfere with a person's life as encounters with similar innocuous mail-boxes produces a stress response, while offering no advantage in avoiding muggings in the future.
The synaptic tagging-and-capture hypothesis alleges a weak stimulus can still create a long-term memory it it's paired with a stronger stimulation entering the nerve through a different synapse.
The changes in the nerve needed for it to store the memory are sparked by chemicals called plasticity-related proteins, which – according to the hypothesis – are 'tagged' in some way at each synapse.
Read more at Science Alert
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