Ciguatera is the most prevalent human seafood poisoning in the world. It is caused by eating seafood containing ciguatoxins, which originate from marine microalgae of the genera Gambierdiscus or Fukuyoa. Ciguatera has affected tropical and subtropical regions for centuries. Recently, the responsible microalgae have reached more temperate climatic zones, including European countries, where cases of ciguatera caused by local fish are reported. The most prevalent and characteristic symptoms of ciguatera are sensory disturbances including unpleasant tingling and painful burning sensations called paresthesiae and dysesthesiae, especially when the skin or mucosae are in contact with cold or cool air, water, drink or food. Itch (pruritus), the unpleasant sensation evoking the urgent need to scratch, is another hallmark symptom of ciguatera. In addition, pain localized in the head (migraine), digestive tract, joints, muscles or teeth are commonly described. All of these ciguatoxin-induced abnormal sensations come from a common cellular target, namely sensory neurons.
There is no specific or effective treatment for ciguatera sensory disturbances. They greatly affect the quality of life, especially when they last for weeks, months or even years, associated with chronic fatigue. In areas endemic for ciguatera, the dietary eviction and marketing ban of the most incriminated seafood species make ciguatera a significant public health and economic concern.
The overall objective of the SENSO-CIGUA project is to better understand the neural mechanisms by which ciguatoxins induce these sensory disturbances in order to ultimately find out bases for specific treatment(s).
In conclusion of the action, the project, which achieved most of its specific objectives, contributed to a significant advance in the state of the art in the field. Using an assay capable of distinguishing between itch and pain-related behaviours, we characterized the behaviours induced by a range of (sub)nanomolar doses of ciguatoxin administered in direct contact with sensory nerves, and studied the involvement of molecular actors. The project also expanded the available knowledge about the subpopulations of sensory neurons activated by ciguatoxin and its ability to sensitize sensory pathways, for example involved in pain and itch.
