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Research and Education Center as a service to professionals, clinicians,
and the public. Funded by a science education grant from the National
Institute on Drug Abuse.
Special thanks to Dr. Erickson, a leader in the
Addiction Science field, for providing these resources to assist in our
efforts to educate and inform many who are need.
Dr. Carlton Erickson,
The College of Pharmacy
UT Austin, Austin TX
78712-1074
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Addiction Sciencean Overview by National Leaders in
Research
Addiction treatment professionals,
medical personnel, social workers, psychologists, law enforcement
personnel, teachers, students, and the general public are often not
aware of the newest research in addiction science. Dr. Erikson is known
for his work and the ability to communicate that to those of us who are
not necessarily scientist, but have a strong concern, and interest in
research, and how it improves the systems we function in.
HopeNetworks, and the organizations partnered and working within our
network, appreciate the permissions granted by Dr. Erickson and efforts
to communicate the latest findings in understandable language.
Nerve Function and Drug Action:
Simplified
CELL SITES OF DRUG ACTION
(A CARTOON VERSION OF HOW CELLS TALK TO EACH OTHER)

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.
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.
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.
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.
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.
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
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 cocaine¼s pharmacological actions.
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.
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!
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.
For further information, please
write or call:
Addiction Science Research and Education Center
Carl Erickson, Director
The College of Pharmacy
UT Austin, Austin TX
78712-1074
512.471.5198
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