Why could the mongoose Rikki Tikki Tavi attack deadly snakes with impunity in Kipling’s “Jungle Book?” Because he has a uniquely mutated receptor for a brain neurotransmitter called acetylcholine, researchers at the Weizmann Institute of Science report in the Proceedings of the National Academy of Sciences.
The toxins in many snake venoms, including that of cobras, bind to the acetylcholine receptors of their victims, blocking nerve-muscle communications. Molecular biologist Sara Fuchs and her colleagues found that the acetylcholine receptor in mongooses—like that in the snakes themselves—is slightly mutated so that the venom simply bounces off the muscle cells, causing them no harm.
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