A prior report suggested that scorpion venom may aid in treating cancer. Well this time it’s the honey bee that comes to the rescue. As a research initiated by two teams from the University of Bristol and the University of Liege in Belgium claim that the apamin which is natural peptide toxin extracted from the venom of the honey bee can help in designing novel treatments to lessen the symptoms of conditions like muscular dystrophy, depression and dementia.
Apamin is known for its ability to block a type of ion channel that allows a high-speed and selective flow of potassium ions out of nerves. The scientists revealed that once these channels are blocked in the brain, the nerves become hyperexcitable and produce improved learning. This activity can possibly display suggestions for the treatment of dementia and depression.
“Drug design depends on knowing the target. Our findings have provided a new approach to designing a therapeutic agent that could help with the treatment of a number of conditions,” quoted Professor Neil Marrion, from the University of Bristol’s Physiology & Pharmacology department.
Also, if apamin is injected it may enhance the symptoms suffered by patients of myotonic muscular dystrophy (MD). The researchers claim that until now the precise mechanism by which apamin acts was not accurately known. The latest research supposedly highlights the results on these KCa2 potassium ion channels, also known as SK channels.
Professor Vincent Seutin, from the GIGA Neurosciences at the University of Liege, quoted, “I am very enthusiastic about the results of our study and I believe that, with the help of this piece of information, the targeting of these channels for the development of future drugs has been made easier.”
Having employed computer models and a genetic approach, the investigators were able to exactly show where apamin binds to block the channel. In order to block ion channels, almost all the molecules act as a plug at their external mouth. The experts explained that apamin blocks by binding away from the channel pore, and causing the shape of the channel to change through an ‘allosteric’ mechanism.
The scientists affirmed that the findings may promote research into the design of new SK channel blockers probably mimicking the action of apamin, to target SK channels in neural and muscular conditions like dementia, depression or MD.
The research is published in the Journal of Biological Chemistry.