ABSTRACT
Marine neurotoxins fall into two general categories, ingestible polyether toxins and contact peptide neurotoxins. The polyether toxins are associated with clinical syndromes (Stommel, 2004) after ingestion of seafoods containing the toxins or the microorganisms that produce the toxins, and include the ciguateric toxins (ciguatoxin, maitotoxin, palytoxin, and scaritoxin), tetrodotoxin (TTX) (puffer# sh or fugu syndrome), saxitoxin (paralytic shell# sh syndrome), and brevetoxins (BTX) (nonparalytic neurotoxic shell# sh poisoning). The actions of these nonprotein toxins are principally directed toward the sodium channel, which can be subdivided into TTX-sensitive channels and BTX-sensitive channels. TTX-sensitive sodium channels are present in peripheral sensory neurons, some motor axons, and along muscle membranes. Along axons, these channels are clustered in high densities at the nodes of Ranvier, with up to 1000 channels per μm2 compared to 25 per μm2 internodally, and are responsible for the propagation of the axonal action potentials. The slower BTX-sensitive sodium channels are found on nociceptive sensory neurons. Alterations of either type of sodium channel may contribute to remodeling, ectopic action potentials, and ephaptic transmissions, resulting in spontaneous sensory disturbances, misperceptions of sensation, and neuropathically mediated pain. Many of the medications we utilize for such pain states modulate neural sodium channels, to include lidocaine, mexiletine, carbamazepine, oxcarbazepine, phenytoin, lamotrigine, topiramate, zonisamide, and tricyclic antidepressants. The ubiquity of such channels make these toxins also suitable for diagnostic purposes.
