Primer: Psychopharmacology, Part I

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.

It’s crazy to think that I’ve been posting these things monthly since last June.  For my first Primer, I talked about Pharmacology, as I had just completed a Ph.D. in it.  Now, a year later, I’ll elaborate further on the subject that got me interested in it in the first place: psychopharmacology.

As I wrote back then, I took a class at Truman State based out of the Psychology department that taught students about psychopharmacology, defined as:

Psychopharmacology — noun

the branch of pharmacology dealing with the psychological effects of drugs.

In broad strokes, we’re talking about how a drug can change your state of perception, whether it causes or alleviates hallucinations, alters your mood, dampens your emotions, and so on.  Something that changes your “normal psychological state” to something else, whether that be therapeutic or “recreational.”

In order to grasp what happens in your brain when your mood is changing, you need to have a basic idea of the structure of the brain and neurotransmission, both subjects I have discussed in the past.  For example, much of your cognition happens in the brain region called the Cerebral Cortex, and it is dependent upon neurotransmitters like acetylcholine and dopamine.  Alternatively, emotions like anger, aggression and fear tend to be centered in another region called the Amygdala.  Bear in mind that the varying areas of the brain “talk” to each other, and if you affect the signaling in one area, you may very well affect another area.  This may well be the point of any pharmacological intervention, but frequently, you get undesired consequences we call “side effects.”

Let’s look at the Cortex first.  Schizophrenia, a disease characterized by delusions, hallucinations and disorganized speech or hearing, is thought to be caused by misfiring neurons in the Cortex that release dopamine.  Therefore, if your cortical neurons are releasing too much dopamine, for any reason, you can end up with hallucinations and delusions, etc.  Interestingly, you can induce schizophrenic-like symptoms in an individual if you give them amphetamine or cocaine, both of which also increase the release of dopamine, though on a wider scale throughout the body.  For those with Schizophrenia, you typically prescribe an antipsychotic, a drug that inhibits dopamine release or reception.

The trick with drugs like antipsychotics, however, is that you want to inhibit dopamine release in the cortex, yet you want to limit that drug’s effect on other areas of the body where you still need dopamine release, or other neurotransmitters like norepinephrine that are responsible for completely different things (hence, side effects).  For example, if you were to design a drug to limit release of dopamine, you could fix their symptoms of Schizophrenia, but you could also affect mobility, as dopamine is responsible for voluntary control of movement.

This is how we arrived at “typical” and “atypical” antipsychotics.  The “typical” drugs were the first-generation antipsychotics that did a reasonable job at limiting schizophrenic symptoms, but also affected other dopaminergic neurons in your body (i.e. your movement).  People on these drugs for decades frequently came down with a movement disorder called Tardive Dyskinesia.  The second generation “atypical” antipsychotics were more specific to the Cortex, and limited schizophrenic symptoms while mostly leaving other dopaminergic signaling pathways alone, thus alleviating dyskinesias.

As another example, Depression is a mood disorder that makes you feel sadness, anxiety, and general hopelessness.  This disease is thought to involve the limbic regions of your brain, which includes the amygdala and the prefrontal cortex.  Depression, however, is opposite of Schizophrenia in that it represents a lack of the neurotransmitters serotonin and dopamine.  The drugs of choice used to be TCAs (tricyclic antipsychotics), a drug that blocked the reentry of serotonin and norepinephrine into neurons, thus prolonging the activity of these neurotransmitters.  In short, it made your serotonin work longer than it usually does, thus alleviating the need for production of more.  As with Schizophrenia, this earlier drug class generated a large number of side-effects because it affected norepinephrine and serotonin throughout the body.  Because TCAs worked on norepinephrine, that also meant that its action would increase in your body, for example, affecting your blood pressure through action on your blood vessels and causing arrhythmias due to action on the heart.  Once SSRIs were developed, they rapidly replaced the TCA drug class because they were more specific toward only serotonin and not norepinephrine.

Both Schizophrenia and Depression are examples of psychological disorders that can be treated effectively with some kind of pharmacological intervention.  Frequently, a given patient will end up trying multiple different drugs over the course of their treatment, and sometimes in various combinations.  Unfortunately, there isn’t a single “silver bullet” for taking care of a given psychological disease, as most people manifest the disorders in different ways, with different drugs being more effective at treating different symptoms.  While an SSRI may prove useful in the short-term, it’s possible a doctor will prescribe a TCA later on after the SSRIs lose their effectiveness.  Antipsychotics act similarly.  And more research is being done on new classes and new modifications to old drugs in order to make them more effective, and especially more selective toward their specific target(s).

The larger point to all of this is that the study of psychopharmacology is an effort to control one’s emotions and behaviors while not affecting the other aspects of their day-to-day life (i.e. side effects).  These drugs typically manipulate neurotransmission to some degree, and hopefully have some kind of selectivity toward specific aspects of a given disease rather than affecting all transmission of that particular compound.  This can be difficult, and can take decades to fully investigate, but it is certainly possible.  As researchers develop more complex maps of the brain, with more detailed pharmacological profiles, new drug classes can be produced that are more specific to a given individual’s needs.

As this is more than long enough, and I still have more to say on the subject, stay tuned until next month when I hit up Part II.

Leave a Reply

Your email address will not be published. Required fields are marked *