The osm-9 mutant strain is defective in the recovery phase of long-term memory dynamics.

Memory by definition is the storage of learned information from experiences where it can be recalled in the future. Memory is essential for organisms of any level, from single celled bacteria to complex mammals like whales in order for them to adapt and survive. The storage of long term memory is known to start in the hippocampus but long-term memory is not simply contained in this one region in the brain but across multiple regions including the cortex, amygdala and nucleus accumbens. This diversity of locations that memory can be located in prompts the question of what molecular components within the nervous system are required to establish and maintain long term memory. To dive into this, we utilize the simple neuroanatomy of C. elegans with only 302 neurons to examine the effects of mutations of specific genes on the success of forming long term memories. Previous work established that C. elegans with defective OSM-9 proteins are unable to sustain an aversion to butanone (an odor that they are innately attracted to) after it is paired once with a negative stimulus. This helped established the importance of OSM-9 proteins for short term memory but how can the OSM-9 protein - a homolog to human TRPV5 and TRPV6 commonly associated with recognising pain and thermoregulation rather than memory - play a part within the dynamics of space training induced long term memory? Here we show that the loss of the OSM-9 protein affects the dynamics of memory consolidation, which is the process by which short term memory is converted to long term memory. Previously, OSM-9 protein was implicated in the formation of short term memory which was termed adaptation. Here, we examine spaced training induced memory that is resistant to re-feeding and depends on sleep. This study indicates that after spaced training, the OSM-9 protein is required for the conversion of short term memory to long term memory and not acquisition. Furthermore, we confirmed that 30 minutes on food after spaced training, Wild type C. elegans seem to lose their memory but gain it back 120 minutes after, emphasizing the dynamics of memory and revealing that it is not a smoothly continuous process. Our results demonstrate that TRPV containing channels plays a role in stabilizing memory for long term use. Analyzing the specific point in which the OSM-9 protein plays a part in reactivating memory may help pave the way to a more detailed understanding of memory dynamics and the processes involved in recovering memory. Future work includes: identifying where the loss of memory goes, whether its masked or truly disappears can further explain what the OSM-9 protein supports when long term memory is formed; understanding if OSM-9 is directly involved with the process of "reviving" the memory or is it involved in the development of the C. elegans circuit which allows for this process to occur.