Addiction Science Research & Education Center

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Presented by faculty at The University of Texas at Austin, Addiction Science Research and Education Center, as a service to professionals, clinicians, and the public.

diagram of a cell

Addiction treatment professionals, medical personnel (physicians, pharmacists, nurses), social workers, psychologists, law enforcement personnel, teachers, students, and the general public are often not aware of the newest research in addiction science.  This website is designed to help scientists educate the above groups to better understand the science of addiction and to overcome myths about drug abuse and addiction. 

In these pages, we discuss topics such as what addiction is and what it is not, the latest theories (and facts) regarding the causes of addiction, methods for treating drug addiction, and ways in which new research is changing our beliefs about how to best control not only all drug addictions, but how to prevent and treat mild and moderate substance use disorders. Much of the information is based upon the second edition of  “The Science of Addiction: From Neurobiology to Treatment”, published in 2018 by W.W. Norton, New York.


Facts and Myths

Accurate information about alcohol and drugs is vital for the public to get a true picture of the role these substances play in public health.  Visit our Facts and Myths page to access detailed information about alcohol and drugs, including 300 facts about alcohol and drugs, 50 drug myths, and diagnostic criteria.

Visit Facts and Myths Page

Communication and Public Speaking

Public advocacy in the addiction field can help generate funding for alcohol and drug research that can benefit victims and their loved ones.  Our Communication Guides page contains a detailed speakers guide aimed at the scientific community, as well as a neurotransmitter role play geared for the classroom setting.

Visit Communication Guides Page

Nerve Function and Drug Action: Simplified

Basic Nerve Function

Cartoon drawing of how neurons communicate

Cell sites of drug action (a cartoon version of how cells talk to each other)

These sections cannot be printed or downloaded without permission of the Director, Carlton Erickson. 

1.  There are millions of cells in the brain. This picture depicts two nerve cells (neurons) and their important components. Nerve Cell One is on the top; Nerve Cell Two is on the bottom.

2.  The large portion of Nerve Cell One is the working part of the cell, also known as the presynaptic area. The presynaptic area is at the end of a sending fiber called an axon, which begins outside the boundaries of the picture in a cell body called the soma. Inside the soma are manufacturing chemicals known as enzymes that manufacture chemicals called neurotransmitters.

3.  These neurotransmitters pass down the axon under the influence of a small electrical current called an action potential. The neurotransmitters are packaged in what look like cellophane envelopes (called vesicles). These vesicles release their contents (neurotransmitters) into the space between the two cells (the synapse), under the influence of small concentrations of calcium ions.

4.  Once in the synapse, one of four things can happen to the neurotransmitters. They either 1) activate an excitatory receptor (on the left), causing Nerve Cell Two to be more likely to fire; 2) activate an inhibitory receptor (middle), causing Nerve Cell Two to be less likely to fire; 3) are “gobbled up” (metabolized) by a monster enzyme (right); or 4) are taken back up into Nerve Cell One (reuptake), repackaged, and sent on down the nerve cell for use later on.

5.  Inside Nerve Cell One is another monster enzyme, known as MAO, which gobbles up the neurotransmitter molecules that accidentally leak out of the vesicles. Outside and above the nerve membrane is a small molecule known as chloride ion, which is necessary for the proper integrity of the vesicle membrane.

6.  Under each of the receptor “ghosts,” is a small rectangle containing globules of substances known as G proteins that are the beginning of a chemical and electrical cascade of events that make Nerve Cell Two more likely (excitation) or less likely (inhibition) to fire and carry the message of Nerve Cell One to the next nervous system component.

(This is a 2-minute course in Neurophysiology!)

Where a Few Drugs Work

1.  Cocaine – It is now known that cocaine acts at the receptor site on Nerve Cell One where reuptake occurs. This is known as the dopamine transporter (abbreviated DAT). Cocaine blocks DAT to cause an increase in dopamine in the synapse, producing the events that eventually lead to the stimulation that is characteristic of cocaine's pharmacological actions.

2.  Amphetamines – Amphetamines act differently than cocaine because they cause an increased release of dopamine (and to some extent other neurotransmitters such as norepinephrine and serotonin). The end result is more dopamine in the synapse (like cocaine), but amphetamine has a more complex pharmacology and works on slightly different brain areas so that its pharmacology is different than that of cocaine.

3.  When either cocaine or amphetamines act on the pleasure pathway of the brain (known as the medial forebrain bundle), the result is a pleasurable or euphoric feeling. When these drugs act on other parts of the brain, other things happen, such as increased muscle movement, jitteriness, increased talkativeness, and even hallucinations. So the part of the brain that is affected by the drug determines the pharmacological actions and side effects, in spite of the fact that the drug works on the same place on the cell in every part of the brain!

4.  Drugs like Prozac work in a fashion similarly to cocaine, but with two main differences. Prozac is a Selective Serotonin Reuptake Inhibitor (SSRI), meaning that it blocks only the uptake of serotonin at the serotonin transporter (SERT). This leads to an increase in serotonin in the synapse to overcome clinical depression, so it works on a different neurotransmitter than cocaine. Also, Prozac acts throughout the limbic system of the brain, which is where we feel our emotions. It does not have a specific and powerful action on the pleasure pathway, which is why it is not addicting. We assume, then, that for something to be able to produce addiction, it must have a major action on the pleasure pathway.