A novel nerve toxin found in a venomous sea snail will give rise to new treatments for a range of brain diseases, scientists predict.

The ability of the poison to lock onto the brain’s nicotine receptors could lead to new medications for “a wide range of disorders including Parkinson’s disease, Alzheimer’s disease, depression, nicotine addiction and perhaps even schizophrenia,” said Michael McIntosh of the University of Utah’s Brain Institute.

Prof McIntosh previously discovered another sea snail toxin or ‘conotoxin’ that was developed into Prialt (ziconotide), a painkiller injected into fluid surrounding the spinal cord to help patients with severe chronic pain and certain nervous system disorders. Prialt, which is sold by Japanese drugmaker Eisai, was approved in late 2004 in the USA and was introduced in Europe last month. Details of the discovery of the new conotoxin from the Pacific snail Conus omaria, will be published on 25 August in The Journal of Biological Chemistry.

Prof McIntosh said the key feature of the substance, called OmIA toxin, was its ability to fit like a key into certain lock-like nicotinic acetylcholine receptors found on cells in the central nervous system. Different forms, or subtypes, of nicotinic receptors control the release of different neurotransmitters. “That’s important because if you had compounds to facilitate the release of one neurotransmitter and not another neurotransmitter, that opens up medicinal potential,” he said. “For instance, one receptor modifies the release of dopamine. There are inadequate amounts of dopamine in Parkinson’s disease, so a medicine designed to fit into a certain subtype of nicotinic receptor would produce more dopamine and thus protect against the development of tremors and other Parkinson’s symptoms.”

A medicine that blocked certain nicotinic receptors could be used to help people quit smoking, and the same method might work for alcoholism because nicotinic receptors may be involved in alcohol addiction, he added. Some nicotinic receptors trigger the release of neurotransmitters involved in memory, so activating the right receptors might lessen Alzheimer’s memory loss. Other nicotinic receptors influence “the release of serotonin and norepinephrine, two neurotransmitters strongly implicated in mood disorders” such as depression, so a drug to activate those receptors might treat depression.

Prof McIntosh said the new toxin itself was unlikely to become a drug because it blocked rather than stimulated nicotinic receptors. But, because it acted on some types of nicotinic receptors and not others – like a key that opens some locks but not others – it had great potential as a tool for precisely identifying the shape and structure of the receptor ‘locks’, thus making it easier to design new medicines or ‘keys’ to fit those receptors and trigger them to release desired neurotransmitters.

He said, however, that it would take at least 10 years to develop new medications based on what is learned from the new toxin. by Michael Day