Life scientists at the University of California, Los Angeles, have discovered that long-term memory in the marine snail can be erased by inhibiting the activity of a specific protein kinase (PKM) associated with memory.

The study may be relevant to veterans of war, rape victims, and people who have seen other horrific crimes.

The scientists studied a simple kind of reflexive memory called sensitization. They administered electric shocks to the snails’ tails. Following this training, when the scientists gently touched a snail’s siphon (an organ in their mid-section used in respiration), the animal responded with a reflexive contraction that lasted about 50 seconds. A week later, when the scientists touched the siphon, the reflex still lasted 30 seconds or more, rather than just the second or two the reflex normally lasts without the shock training. This constituted a long-term memory.

Once the marine snail had formed the long-term memory, the scientists injected an inhibitor of PKM into the snail and 24 hours later touched the siphon; the marine snail responded as though it had never received the tail shocks, with a very brief contraction. The long-term memory was gone, the researchers said.

They also removed key neurons from the snail’s nervous system associated with sensitization and put them in a Petri dish, recreating a two-neuron “circuit” (a sensory neuron and a motor neuron). By inhibiting PKM, they succeeded in erasing a long-term memory in the circuit in the dish. They are the first scientists to show that long-term memory can be erased at a connection between just two neurons.

The research has important potential implications for the treatment of post-traumatic stress disorder, as well as drug addiction (in which memory plays an important role), and perhaps Alzheimer’s disease and other long-term memory disorders, the researchers said.

Ref.: D. Cai, K. Pearce, S. Chen, D. L. Glanzman, Protein Kinase M Maintains Long-Term Sensitization and Long-Term Facilitation in Aplysia, Journal of Neuroscience, 2011; 31 (17): 6421 DOI: 10.1523/JNEUROSCI.4744-10.2011