Nicotine, the addictive agent in cigarettes, comes from the leaves of tobacco plants (Nicotiana). Plants, of course, do not manufacture nicotine as a favor to smokers, but for their own benefit: nicotine is one of the most powerful insecticides in the world, highly effective at stopping hungry, leaf-munching pests in their six-footed tracks.
Nicotine is a neurotoxin, and to understand how it works, you’ll need to understand a few things about the nervous system. Nerves are simply long, thin cells that run through your body, carrying signals as electrical impulses. Here’s the problem: at the junction between two nerve cells, or between a nerve and a muscle cell, there’s a space across which electrical impulses cannot travel. This space is called the synapse.
To keep the message going, the signal-sending nerve cell sends out an army of molecules called neurotransmitters, who boldly drift across the synapse like astronauts from space-ship to satellite. When a neurotransmitter arrives at the receiving nerve or muscle cell, it enters through a tube-shaped receptor molecule.
There are many kinds of neurotransmitters, each with its own unique receptor. Take acetylcholine, which carries signals from nerve cells to muscle cells. When you recoil from a hot stove, it’s acetylcholine that tells your muscles to get moving.
If a poison kept all your acetylcholine receptors closed, you would be paralyzed: your muscles wouldn’t get any signals from the nervous system. If, on the other hand, the toxin kept receptors constantly open, your muscles would be constantly trying to move. You would go into convulsions, unable to control your body. Eventually you would exhaust yourself and die.
That’s how nicotine works (Zevin et al. 1998). In small doses, like in a cigarette, it works as a mild stimulant, keeping a few more receptors open than usual. In massive doses, like when a caterpillar eats a tobacco leaf, it works like a doorstop, keeping all acetylcholine receptors wide open. The unfortunate insect convulses, contracting all its muscles simultaneously until it runs out of energy and expires.
For many years, farmers used nicotine as a pesticide, spraying it over their crops to poison any hungry insects. However, nicotine is quite toxic to mammals, including humans. It isn’t sold as a pesticide anymore in the U.S. or Europe, replaced by neonicotinoids. The new pesticides are similar to nicotine, highly effective, and work in the same way, but are safer for people (not insects, of course).
There are insects that eat tobacco leaves, and those insects have acquired an immunity to nicotine. The best-known example is the tobacco hornworm (Manduca sexta), a big, fat, bright green caterpillar that ultimately transforms into a hawkmoth. In fact, these caterpillars have evolved the ability to store nicotine in their own bodies, making themselves toxic to caterpillar-eating predators. Experiments have shown that wolf spiders normally avoid tobacco hornworms, but if the caterpillars are fed a diet lacking in nicotine, the spiders attack without hesitation (Kumar et al. 2013).
Kumar P., S.S. Pandit, A. Steppuhn, and I.T. Baldwin. 2013. Natural history-driven, plant-mediated RNAi-based study reveals CYP6B46’s role in a nicotine-mediated antipredator herbivore defense. Proceedings of the National Academy of Sciences U.S.A. 111(4): 1245-1252.
Zevin S., S.G. Gourlay, and N.L. Benowitz. 1998. Clinical pharmacology of nicotine. Clinics in Dermatology 16(5): 557-564.