Learning about how the nervous system works isn't easy, and learning about learning and memory formation is particularly tricky. Fortunately, studies on molluscs and other invertebrates have proved particularly useful in dissecting the neural and molecular machinery for learning and memory formation. But once formed, memories are not necessarily permanent and might need consolidating over time. A recently recalled memory may be particularly fragile and may need reconsolidation. In a recent paper published in J. Neurosci., Susan Sangha, Ken Lukowiak and colleagues investigated the mechanisms underlying this reconsolidation. Turning to their favourite experimental animal, the pond snail Lymnaea stagnalis, they asked if memories are so fragile after being recalled that, without reconsolidation, they will be erased.
Lymnaea can breathe through their pseudosome (or respiratory orifice) as well as through their skin. Sangha and colleagues put this talent to use in their experiments. The snails were placed in beakers of water through which N2 was bubbled to make it hypoxic. The snails climb to the surface to breathe through their pseudosome when they run out of oxygen. By gently prodding the pseudosome they can be taught to breathe through their skins and can even remember this lesson for days or weeks. This memory is stored in the same network of neurones that produces the breathing.
But what happens when encountering the same set of circumstances jogs the snail's memory? When exposed to the same hypoxic conditions, the snails recall their original training and remember not to breathe. But, since reawakened memories may be particularly fragile, Sangha and colleagues asked whether the reactivation of this memory meant that it now had to be reconsolidated. To do this they reactivated the memories of one half of the snails that were originally trained. They then exposed all the trained animals to one of three memory-disrupting treatments. Some animals were cooled, a commonly used method of memory disruption, whereas other animals were injected with actinomycin D,blocking the synthesis of new RNA and disrupting the production of new proteins involved in memory formation. In the third group of trained animals,the cell body of a neurone within the breathing network, RPeD1, was removed,also preventing new RNA and protein synthesis.
Four hours after the treatment the animals were tested to see whether they still remembered to keep their pneumostomes shut when they got breathless. Only those snails that had had their memories reactivated showed impairment in their performance - they started to use their pneumostome to breathe at the air-water interface again.
These results suggest that the impaired memory was contingent on memory reactivation and requires new RNA/protein synthesis and the cell body of RPeD1. Combining these results with previous work from Lukowiak's laboratory,which showed that memory consolidation is also dependent upon RNA/protein synthesis and the cell body of RPeD1, makes us wonder whether similar mechanisms underlie both memory consolidation and reconsolidation. One way to get closer to an answer to this question would be to determine if the same genes are transcribed and translated during memory consolidation and reconsolidation. Another obvious link lies between reconsolidation and forgetting. Is it possible that reconsolidation provides an opportunity to forget previously formed memories and overwrite them with new ones?Lymnaea is proving an excellent model system for studying the mechanisms underlying memory formation in a simple neural network, and the answers to these and other questions may not be too far away.
