SUMMARY
Memory is one of the most important abilities of the brain. It is defined as an alteration in behavior from an experience. For example, the C. elegans nematode will downregulate its chemotactic response to an innately attractive odor if it is not paired with food. This process is an example of olfactory classical conditioning. Through spaced training with this odor in the absence of food, C. elegans will maintain this memory of the odor for a prolonged period of time, akin to long-term memory formation. Although TRP channels are classically thought of as primary sensory receptors, intriguingly, it has been reported that the OSM-9/TRPV5/TRPV6 (TRP vanilloid) channel is required for odor short-term memory. We have discovered a new role for osm-9/TRPV in long-term olfactory memory formation (LTM). The osm-9 mutant animals can acquire memory of the conditioned stimulus (odor) just like wild-type, but are unable to consolidate the memory for long-term maintenance. Interestingly, this TRPV-mediated long-term memory does not require sleep to form the long-lasting memory. Additionally, we found that genomic DNA and not cDNA is able to rescue the short-term odor memory defects seen in the null mutants. TRP channels are well studied in their ability to sense noxious stimuli, yet they are also implicated in memory and many diseases and disorders that limit neural plasticity, including Parkinson’s disease, Alzheimer’s disease, stroke, and sense disorders including anosmia. Our studies uncovered a role of TRP channels in neural plasticity, specifically, in olfactory long-term memory formation. These findings will broaden our knowledge of TRP channel function as a mediator of plasticity and memory, which could also potentially aid in understanding and treating the many diseases and disorders caused by TRP channel dysfunction.
Competing Interest Statement
The authors have declared no competing interest.
