How does nicotine affect neurons and neurotransmitters?

One of the primary effects of nicotine is to alter the way that neurons (i.e., brain cells) communicate. Neurons communicate with each other through both electrical and chemical signals. Each neuron consists of a cell body (the main part of the neuron that contains the nucleus, or the cell’s control center), an axon, and many dendrites. The axon is one long extension from the cell body that carries electrical signals from one end of the neuron to the other end (referred to as the terminal). These signals travel extremely fast–up to hundreds of miles per second. Dendrites are shorter extensions that also branch off the cell body. Think of the dendrites as tree roots that branch out. The dendrites receive signals from other neurons in the form of chemicals.

Neurons communicate information to each other when they are in close contact. The connections between neurons are called synapses. On average, one neuron can form about 1,000 synapses with other neurons. With millions of neurons forming thousands of neural connections, it is estimated that the number of neuron-to-neuron connections in the brain exceeds the number of stars in our galaxy.

So how does the communication work at the synapse? First, an electrical impulse travels down the axon toward the terminal. Once there, the electrical signal triggers the release of chemicals called neurotransmitters from tiny sacs into the synaptic space outside the terminal. These chemicals actually carry the “messages” from one neuron to another. Once in the synaptic space, the neurotransmitter attaches to specific proteins called receptors on the dendrites of the neighboring neuron. There are thousands of receptors on the dendrites, with each type of receptor recognizing only a very specific neurotransmitter, similar to a lock and key. When the neurotransmitter binds (or attaches) to a specific receptor, the receptor will either increase or decrease the electrical activity of the neuron on which it resides.Let’s consider one of the major neurotransmitters in the brain called acetylcholine. Interestingly, nicotine mimics this neurotransmitter. Nicotine acts just like acetylcholine, but works even better. This is described below. Acetylcholine binds to receptors (“acetylcholine receptors”) that increase the electrical activity of neurons, resulting in more signals transmitted to neighboring neurons. Once acetylcholine has done its job, it is destroyed. New acetylcholine must be made by the cells to repeat the whole process.

As previously mentioned, nicotine mimics the effect of the neurotransmitter acetylcholine. When nicotine enters the brain, it can actually bind to the same receptors that bind acetylcholine. For this reason, the acetylcholine receptor is often referred to as a nicotinic receptor.

However, when one uses a tobacco product or another nicotinecontaining product, there is more nicotine available in the synaptic spaces compared to acetylcholine. The nicotine competes with acetylcholine to bind to the nicotinic receptors and it wins. Now, with more nicotinic receptors activated by nicotine, a more intense response is produced.

So while acetylcholine normally provides the just the right amount of alertness when it binds to its receptors, nicotine produces a much more intense response (increased alertness, pleasurable feelings) due to its higher concentrations at the acetylcholine receptors.

Nicotinic receptors are found in many other regions of the body besides the brain. Not surprisingly, nicotine acts in the body wherever nicotinic receptors are found, such as on the heart, blood vessels, and muscles. The widespread distribution of nicotinic receptors explains why nicotine will increase heart rate, blood pressure, and muscle contractions.

What happens with continued use of nicotine?

When one continues to use a product with nicotine in it, a strange thing happens. The number of nicotinic receptors—that is, acetylcholine receptors—increases on the neurons! With more receptors present, the person needs more acetylcholine binding to them to feel normal. But the neurons can only make so much acetylcholine. So what is the result? The person needs more nicotine to feel normal.

When the nicotine is not present, a person will often get symptoms such as headaches, tremors, shakiness, and an overall feeling of irritability and frustration. To get rid of these “withdrawal” symptoms, the user will smoke another cigarette or use another tobacco product and begin to feel much better. The presence of withdrawal symptoms is typical of dependence and it almost always precedes addiction.

In addition, the increased nicotinic receptors can also explain tolerance, or the need to use more of the product containing nicotine to get the original effect.

Can receptors recover from nicotine exposure?

The good news is that the increase in receptor number is probably not permanent. Once one stops using a product containing nicotine, the number of receptors will return to normal pre-nicotine levels—although this could take more than a year. However, immediately after stopping smoking for example, many users experience unpleasant withdrawal symptoms because the brain now has an excess of nicotinic receptors, which are unoccupied. The long process for the brain to recover to normal is one reason why many people who try to quit using nicotine products can’t get past the first year (or even week!) nicotine-free.