Honey, aloe, frankincense oil, almond oil, mucilage paper—these were all ancient remedies for the age-old problem of wrinkles. But a bacterial toxin of which five hundred grams could kill the entire human race? Though it sounds more like a terror plot from a Hollywood doomsday movie, such a deadly substance is, in fact, the most modern weapon available in the pharmaceutical industry’s persistent fight against “signs of aging.” Botox—injected into the faces of hundreds of thousands of Americans each year, it is one of the deadliest toxins on earth. To understand how it functions on a microscopic level is to realize just how desperate its proponents are to erase from their foreheads any evidence of the passage of time.
To move, or not to move, that is the question—or at least, the question Botox addresses within a muscle cell. As a toxin, Botox immobilizes muscles by interrupting a fundamental process: the communication between that muscle’s cells and its motor neurons. Think of a motor neuron as a telephone line transmitting instructions, in the form of electrical signals, from the brain to an individual cell. Instructions given by motor neurons to muscles cells initiate every movement a person makes, from waving an arm, to blinking an eye, to furrowing a brow. But a motor neuron and the muscle cell that it is “phoning” never actually touch to transmit the electrical signals. Instead, they are separated by a gap roughly the width of 1/5000th of a human hair. A motor neuron and a muscle cell positioned across such a gap from one another form a “neuromuscular junction.” At these junctions, for an instruction to pass from the neuron to the cell and make the cell move, the instruction must jump the gap.
Enter acetylcholine, a chemical molecule that, when it comes in contact with a muscle cell, causes the cell to contract. At the neuromuscular junction, a motor neuron on its side of the gap branches into what look like the fingers of a frog perched on a twig. In each froglike fingertip are hundreds of balloons, or “vesicles,” filled with acetylcholine. When a motor neuron receives an electrical signal from the brain, the signal prompts the balloons to fuse with the neuron’s membrane, releasing acetylcholine into the gap through the neuron’s “fingertips.” The acetylcholine crosses the gap, reaches the muscle cell and transmits its “contract” command. The way Botox alters the normal activities at the neuromuscular junction is simple: it prevents the balloons from fusing with the membrane of the neuron and thus, from releasing acetylcholine. Administered to the face, Botox stills the muscles that create expression, and by extension, wrinkles.
If the paralyzing effects of Botox sound familiar, it’s possible you learned about them in connection with spoiled food. Botox is a variation of the same botulinum toxin that, when consumed in the form of uncooked canned goods, results in a painful death by stilling the muscles of the lungs. Its lethal possibilities fire the imagination. While governments have actually experimented with botulinum toxin as a potential weapon of warfare, a more colorful—and uncorroborated—rumor suggests that the CIA once tried to assassinate Fidel Castro with a botulinum-laced cigar. What most people don’t realize is that spores of the bacteria that cause botulism–Clostridium botulinum—exist all around us on the surfaces of fruits and vegetables, on seafood and in the soil—albeit in minute and innocuous quantities.
From a neuromuscular perspective, a botulinum toxin is a straightforward substance—be it administered by a murderer or a cosmetologist, it will act upon the neuromuscular junction in exactly the same way. Understanding how the junction works proves, in the case of Botox, that the difference between causing death and simulating youth is only a matter of degree. The junction’s processes also help to illustrate, though they cannot answer, the larger question Botox poses: Why are we humans so willing to risk bodily harm for the sake of beauty?
Meehan Crist, Clay Lacefield, Kim Tingley