at least four different genera of cyanobacteria and has been reported in north america, europe, africa, asia, and new zealand. toxic effects from anatoxin-a progress very rapidly because it acts directly on the nerve cells (neurons) as a neurotoxin. the progressive symptoms of anatoxin-a exposure are loss of coordination, twitching, convulsions and rapid death by respiratory paralysis. the nerve tissues which communicate with muscles contain a receptor called the nicotinic acetylcholine receptor. stimulation of these receptors causes a muscular contraction. the anatoxin-a molecule is shaped so it fits this receptor, and in this way it mimics the natural neurotransmitter normally used by the receptor, acetylcholine. once it has triggered a contraction, anatoxin-a does not allow the neurons to return to their resting state, because it is not degraded by cholinesterase which normally performs this function. as a result, the muscle cells contract permanently, the communication between the brain and the muscles is disrupted and breathing stops. external video very fast death factoruniversity of nottingham the toxin was called the very fast death factor because it induced tremors, paralysis and death within a few minutes when injected into the body cavity of mice. in 1977, the structure of vfdf was determined as a secondary, bicyclic amine alkaloid, and it was renamed anatoxin-a. structurally, it is similar to cocaine. there is continued interest in anatoxin-a because of the dangers it presents to recreational and drinking waters, and because it is a particularly useful molecule for investigating acetylcholine receptors in the nervous system. the deadliness of the toxin means that it has a high military potential as a toxin weapon. cylindrospermopsins cylindrospermopsin cylindrospermopsin (abbreviated to cyn or cyl) was first discovered after an outbreak of a mystery disease on palm island in australia. the outbreak was traced back to a bloom of cylindrospermopsis raciborskii in the local drinking water supply, and the toxin was subsequently identified. analysis of the toxin led to a proposed chemical structure in 1992, which was revised after synthesis was achieved in 2000. several variants of cylindrospermopsin, both toxic and non-toxic, have been isolated or synthesised. cylindrospermopsin is toxic to liver and kidney tissue and is thought to inhibit protein synthesis and to covalently modify dna and/or rna. there is concern about the way cylindrospermopsin bioaccumulates in freshwater organisms. toxic blooms of genera which produce cylindrospermopsin are most commonly found in tropical, subtropical and arid zone water bodies, and have recently been found in australia, europe, israel, japan and the usa. saxitoxins saxitoxin saxitoxin (stx) is one of the most potent natural neurotoxins known. the term saxitoxin originates from the species name of the butter clam (saxidomus giganteus) whereby it was first recognized. saxitoxin is produced by the cyanobacteria anabaena spp., some aphanizomenon spp., cylindrospermopsis sp., lyngbya sp. and planktothrix sp., among others). puffer fish and some marine dinoflagellates also produce saxitoxin. saxitoxins bioaccumulate in shellfish and certain finfish. ingestion of saxitoxin, usually through shellfish contaminated by toxic algal blooms, can result in paralytic shellfish poisoning. saxitoxin has been used in molecular biology to establish the function of the sodium channel. it acts on the voltage-gated sodium channels of nerve cells, preventing normal cellular function and leading to paralysis. the blocking of neuronal sodium channels which occurs in paralytic shellfish poisoning produces a flaccid paralysis that leaves its victim calm and conscious through the progression of symptoms. death often occurs from respiratory failure. saxitoxin was originally isolated and described by the united states military, who assigned it the chemical weapon designation "tz". saxitoxin is listed in schedule 1 of the chemical weapons convention. according to the book spycraft, u-2 spyplane pilots were provided with needles containing saxitoxin to be used for suicide in the event escape was impossible. aetokthonotoxin transmission from cyanobacteria to the bald eagle aetokthonotoxin (abbreviated to aetx) was discovered in 2021 as the cyanobacterial neurotoxin causing vacuolar myelinopathy (vm). as the biosynthesis of aetokthonotoxin depends on the availability of bromide in freshwater systems and requires an interplay between the toxin-producing cyanobacterium aetokthonos hydrillicola and the host plant it epiphytically grows on (most importantly hydrilla), it took > 25 years to discover aetokthonotoxin as the vm-inducing toxin after the disease has first been diagnosed in bald eagles in 1994. the toxin cascades through the food-chain: among other animals, it affects fish and waterfowl such as coots or ducks which feed on hydrilla colonized with the cyanobacterium. aetokthonotoxin is transmitted to raptors, such as the bald eagle, that prey on these affected animals. vacuolar myelinopathy is characterized by widespread vacuolization of the myelinated axons (intramyelenic edema) in the white matter of the brain and spinal cord. clinical signs of the intoxication include the severe loss of motor functions and sight. affected birds fly into objects, lack coordination in swimming, flying and walking, develop tremors of the head and lose their responsiveness. as the toxin has been shown to bioaccumulate, there is concern that it might also be a threat to human health. however, toxicity to mammals has yet to be confirmed experimentally. aetokthonotoxin lipopolysaccharides lipopolysaccharides are present in all cyanobacteria. though not as potent as other cyanotoxins, some researchers have claimed that all lipopolysaccharides in cyanobacteria can irritate the skin, while other researchers doubt the toxic effects are that generalized. amino acids bmaa the non-proteinogenic amino acid beta-methylamino-l-alanine (bmaa) is ubiquitously produced by cyanobacteria in marine, freshwater, brackish, and terrestrial environments. the exact mechanisms of bmaa toxicity on neuron cells is being investigated. research suggests both acute and chronic mechanisms of toxicity. bmaa is being investigated as a potential environmental risk factor for neurodegenerative diseases, including als, parkinson's disease and alzheimer's disease. gallery other cyanotoxins: guanitoxin aplysiatoxin