Madam Fathom has an excellent discussion of nicotine’s effect on the brain and cognitive function. First off, I’ve rarely seen a clearer explanation of how neurons actually work:
Neurons are functionally integrated in expansive neural networks, with each neuron receiving up to thousands of inputs from other neurons. However, the neurons are not actually physically connected to one another; there is a tiny gap that separates neurons, called a synapse.
When a neuron is activated, an electrical pulse (an action potential) travels down its membrane; the neuron is said to “fire” an action potential. When the action potential reaches the end of the neuron, it cannot traverse the synapse, but instead induces the release of chemicals which can. Once liberated from the “pre-synaptic” neuron, these chemicals (called neurotransmitters) navigate across the synapse and bind to specific receptors on the “post-synaptic” neuron. Once bound, the neurotransmitters induce one of many physiological changes: they can make it easier to fire an action potential (“excitatory” neurotransmitters), more difficult to fire an action potential (“inhibitory” neurotransmitters), or modulate the firing rate or other behavioral properties of the cell.
An overwhelming number of pre-synaptic neurons, all of which are sources of neurotransmitters, impinge on a single post-synaptic neuron, yet the latter responds with a binary decision: fire or don’t fire. The cell creates order from this chemical deluge by performing a complex, time-dependent summation of all of its inputs; if it receives a sufficient number of excitatory inputs within a reasonable time window, it will fire an action potential and release its own neurotransmitter, passing the information along the circuit.
Why can’t all science writers be this clear? She goes on to explain how nicotine affects this process:
Each neurotransmitter can bind to a number of complementary receptors. One of the receptors for a neurotransmitter called acetylcholine (ACh) happens to also bind and respond to nicotine, which is not naturally present in the body. Thus when a post-synaptic neuron containing these particular receptors (called nicotinic ACh receptors, or nAChRs) is exposed to nicotine (as in when someone smokes a cigarette), it behaves as if it has been influenced by ACh; i.e. to an individual nAChR, nicotine and ACh are indistinguishable.
The problem, of course, is that while each individual neuron is independently in charge of acetylcholine delivery, nicotine affects the entire brain simultaneously. Depending on the individual brain, this can have positive or negative consequences. Madam Fathom goes on to discuss the current state of research on using nicotine to accentuate those positive consequences, for treatment of Alzheimer’s, Parkinson’s, and other disorders, and explain what needs to be done next.
In my view, giving Madam Fathom a book contract wouldn’t be a bad next step!
Read her whole post.