In this unit, the underlying concepts that define addiction will be
examined. The models of addiction introduced in Unit 1 are reviewed in
more detail and a helpful summary can be found in the text (Lewis,
2014, pp. 24–25). The models outlined provide a context for
understanding the dynamics of addictions. The relative importance of
issues related to environmental, psychological, biological, genetic,
and systemic factors are given varying levels of importance in these
models. The models of addiction can help explain the focus of various
treatment approaches that will be explored in this course and
encountered in scholarly literature. Defining what addiction involves
is necessary before assessment and treatment can be attempted.
Terminology relevant to addictions is also explored. It can support a
foundational knowledge necessary to read and interpret scholarly
literature. Pharmacological concepts and details of neuroanatomy may
require repetition and review to master. Additional resources, in the
form of media, are included in the study activities to offer more
opportunities to review the role of neurological structures and
Lewis, T. (2014). Substance abuse and addiction treatment: Practical
application of counseling theory. Upper Saddle River, NJ: Pearson.
To successfully complete this learning unit, you will be expected to:
1. Analyze current research addressing models of addiction.
2. Analyze the role of biological contributions to addiction theory.
Unit 2 Study 1
Use your Substance Abuse and Addiction Treatment text to read the
• Chapter 2, “Terms, Models, and Ethical Issues in Substance Abuse
Addiction,” pages 16–31.
Use the Internet to read the following articles from the National
Institute of Drug Abuse:
• “Drugs, Brains, and Behavior: The Science of Addiction.”
• “Commonly Abused Drugs Chart.”
View the animation Neurotransmitters to learn how a chemical substance
in the body carries signals from one nerve cell to another. The
Nerve cells, or neurons, in the brain aren’t connected to each other.
For communication between neurons to occur, molecules must deliver
information across a small gap between neurons. This gap is called a
The molecules that transmit information, called neurotransmitters,
must leave the original neuron, enter the synapse, and bond with the
receptors on the adjacent neuron. The neuron that releases the
neurotransmitters is called the presynaptic neuron. The neuron that
receives the neurotransmitters is called the postsynaptic neuron.
Let’s look at how this communication process actually takes place.
Neurotransmitters, such as serotonin and dopamine, are manufactured in
the cell body of the presynaptic neuron.
Once manufactured, the neurotransmitters travel down the axon of the
neuron to the terminal bouton.
The neurotransmitters are stored in the terminal bouton in small
containers called vesicles until they are ready for action.
When action occurs in the dendrites of a neuron, this triggers the
release of the neurotransmitters from the vesicles. The
neurotransmitters move toward the membrane, or outer edge, of the
terminal bouton and then fuse with the membrane.
For a split second, tiny openings appear in the membrane.
Through these tiny openings, the neurotransmitters in the vesicles are
released into the synapse.
This release allows the neurotransmitters to travel across the synapse
toward the receptors on the membrane of the postsynaptic neuron.
When neurotransmitters are released into the synapse, three things can
happen. Some neurotransmitters bind with the receptors on the membrane
of the postsynaptic neuron, as shown here. When this happens,
communication between neurons occurs.
However, some neurotransmitters are destroyed when released into the
Others are absorbed by a reuptake transporter pump. In this case, the
neurotransmitters return to the presynaptic neuron and are once again
stored in the tiny vesicles inside the terminal bouton. Let’s look at
an example of how psychotropic medication can help the communication
process when it malfunctions. To understand this example, let’s first
define excitatory and inhibitory neurotransmitters.
Excitatory neurotransmitters activate or excite adjacent neurons on
the receptor membrane.
Inhibitory neurotransmitters stop or reduce action on the receptor
Let’s use aggression in our example. Aggression can be due to
deficient re-uptake of certain neurotransmitters, like serotonin. We
can visualize how a surplus of serotonin can be excitatory. Thus, a
medication that is excitatory, instead of inhibitory, blocks the
neurotransmitters from binding with the receptors and instead, returns
them to the presynaptic neuron for storage in the vesicles.
Based on this information and your readings, consider the following
questions. Can you envision how a medication could be used to
pharmacologically inhibit aggression of repeat violent offenders? Can
an effective and ethical violence treatment program be developed based
on such a medication?
Discussion 1: 1 page needed with minimum of 250 words and 2
Role of the Brain in Addiction
Select two models of addiction from the chart appearing on pages
24–25 in the Lewis text. Compare how each model addresses the brain
changes (neurological effects) associated with using a substance (or
gambling) to excess. (Note that the media pieces and optional articles
may be helpful to aid your understanding of the role of the brain in
addiction.) Consider the relative emphasis that each model places upon
the role of physiological brain functions or changes to explain
addiction. Make an educated prediction regarding how well the model
can adapt to emerging developments in the neuroscience of addiction.
Discussion 2: 1 page needed with minimum of 250 words and 2
Models of Addiction and Current Treatment
Locate an article in the library written within the last five years
that describes a specific treatment for an addictive disorder.
Identify which model of addiction would be most consistent with that
treatment approach. If no single model appears to help explain the
assumptions about addiction underlying that treatment, select the
aspects of the two models that come closest. How does that model
support current treatment approaches?
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