Primer: Neurotransmission

These posts, tagged “Primer,” are posted for two reasons: 1). to help me get better at teaching non-scientists about science-related topics; and 2). to help non-scientists learn more about things they otherwise would not.  So, while I realize most people won’t read these, I’m going to write them anyway, partially for my own benefit, but mostly for yours.

As I’ve mentioned…oh…countless times, I became interested in my chosen field primarily because of a class titled “Psychopharmacology,” offered by the Psychology Department at Truman.  As the name suggests, the class primarily focused on how drugs modify an individual’s mental state, whether it’s an illicit drug that changes the way you act (e.g. methamphetamine), or one that’s used to help you cope as you carry out your day (e.g. diazepam [Valium]).

Back in June, I posted about Pharmacology, the study of how a drug acts within an organism.  One thing I discussed, but did not elaborate on, was that many drugs function at receptors, and the modification of these receptors is what gives you the desired effect of said drug.  However, in order to understand how these receptors actually do something to your body, you need to understand the basics of how neurotransmission works.

Basically, neurotransmission is a signal sent between two specialized cells called neurons.  These cells make up a large portion of the brain (i.e. there are other cell types, including astroglia and microglia) and provide all the processing power you need to carry on with whatever task you wish.  Therefore, if you want to modify something about that task, these are important cells to consider and/or target with a drug.  Neurons take advantage of channels in their membranes that allow selective transfer of ions like sodium, potassium, chloride and calcium.  When these ions cross the membrane from outside the neuron to the inside (or vice versa), an electrical charge is produced.  These channels open and close selectively to allow certain things through, and keep other things out.  For example, sodium channels in neurons typically allow sodium into the cell, while potassium channels tend to allow potassium to leave the cell.

Many of the receptors that drugs are targeted toward are channels, or the drug-targeted receptors somehow affect the ability of channels to open or close.  Therefore, if you can target your drug toward a specific channel, you can keep it open longer, or close it sooner, allowing you to affect whether a neuron is able to continue propagating its signal.

So, the electrical signal caused by transfer of ions across a neuron’s cell membrane (or “action potential“) travels down the neuron, from end to end.  On one end is the “cell body” (or “soma”) and on the other end is the “axon terminal.”  The electrical signal always goes from the cell body to the axon terminal.  The cell body is covered in “dendrites,” outcroppings of the cell that receive a signal from another neuron’s axon terminal.  Therefore, typically, (1) a signal will start at the dendrites; (2) travel down the axon; (3) trigger a set of events in the axon terminal resulting in (4) the release of a neurotransmitter that (5) crosses the synapse until it reaches another dendrite and (1) starts the process over again.

What happens between the axon and the dendrite can best be described by this image, stolen from Wikipedia:

Neurotransmitters are packaged in “vesicles” that are directed to release their contents into the synaptic cleft where they travel across the cleft to the opposing dendrite, setting off a similar cascade in the next neuron.  There are also “reuptake transporters” in the cleft to help remove excess neurotransmitter, so you don’t have that opposing neuron continuing to fire too long.

Examples of neurotransmitters include dopamine, adrenaline (epinephrine), acetylcholine, nicotine and serotonin.

Now, you probably recognize a few of those neurotransmitters, right?  For example, you probably know that serotonin happens to be very important to your mood.  If you don’t have serotonin, you tend to get depressed.  So what can you do to help combat this deficiency?  Try taking an SSRI (selective serotonin reuptake inhibitor).  That drug targets the “reuptake transporter” in the cleft, allowing the serotonin you’re already making to stay in the cleft longer, helping to activate those neurons to keep your mood a bit happier.

You’d use an SSRI to help serotonin to reach its target neuronal receptors, thereby allowing for increased signal propagation through neurons.  But what if you want to limit propagation of signals, for example, in the case of an epileptic seizure when neurons are firing uncontrollably?  You can use a depressant like carbamazepine.  This drug targets channels and modifies them in such a way that the electrical signal (“action potential“) being sent down the axon is limited, or “depressed.”  It prevents the signal from continuing and, therefore, less (or no) neurotransmitter is released into the synapse.  That same drug can be used to help treat the manic symptoms of bipolar disorder, as well.

So, all of these principles are taken into account (as well as countless others…) when looking for drug targets, and when doctors are prescribing medications.  This is why you can have so many complications when you are prescribed a cocktail of medications, especially when you get older.  If you are taking, say, 10 different medications per day, prescribed by different doctors, it is easy for at least one of those drugs to counteract the effects of another.  There are many factors to consider when prescribing or taking these kinds of medications, as they have effects all over the body.  One simple example is methamphetamine.  This drug targets that reuptake transporter, much like an SSRI does, but it (1) does so for a class of neurotransmitters called catecholamines, and (2) reverses the transporter, rather than blocks it.  The class of catecholamines include dopamine and adrenaline.  So, if you take methamphetamine, you will be increasing the amount of dopamine and adrenaline in your body, not just your brain.  Your heart races because of the adrenaline, and the psychological effects occur because of the dopamine (including its addictive qualities).

In summary, neurotransmission is pretty complicated, but its basics are understandable.  The take-home concepts are:

  • Neurons are responsible for “processing” in your brain, and they use electrical and chemical signals to communicate with each other
  • Many drugs that affect your psychology target the ability of neurotransmitters to “continue the signal” from neuron to neuron
  • Some drugs affect more than one aspect of neurotransmission, and in more than one location

4 thoughts on “Primer: Neurotransmission”

  1. why would I be taking 20 pills a day? In 40 yrs I’ll be 90! That’s really old. I probably wouldn’t be able to swallow 20 pills in a day.
    Anyway – we’re not reading this one. Sorry. Just glad you’ll be earning the big bucks and will be taking care of us in 40 years! Thank you bushk!

  2. Just the direction things are going, Mom. There’ll be more and more “combination pills” of existing, off-patent drugs (just so the companies can re-package, re-patent, and re-sell them to you). People tend to want a “quick fix” for their problems, so pills are the most convenient and easy way to take care of things!

    And I’m hoping Meg can take care of ME in 40 years. I’ll be in my upper 60s by then, after all. Although, the retirement age will probably be 75 by then. 😛

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