Drug addiction has been a
conflicting issue for years: is it a culture of mentality, or are there truly
physical differences or changes that occur in addicted individuals? For years,
scientists were limited to observing behavior related with addiction, which
then developed to observing chemical changes in the body. Observing the
chemical response to pleasure/pain stimulation has provided great insight into
the study of the affects of drugs. The major chemical process involved in drug
addiction is that of the dopamine reward system.
Researchers studying the reward
system in the brain have found that the neurotransmitter dopamine plays a major
role. Both natural rewards, such as sex
or chocolate, and artificial rewards, such as cocaine or morphine, activate the
dopamine system in similar ways. Behaviors are reinforced or rewarded partially
due to the release of dopamine in the structures of the brain that are part of
the neuron known as the “synapse”. The dopamine is then removed from the
synapse by dopamine transporters. The “high” that comes from cocaine is due to
the blockage of the re-uptake of dopamine by the dopamine transporters. This
increases the excitation and makes the pleasing affects of dopamine last
longer. This information gives insight to the chemical implications of cocaine
use, but it does not shed much light into the process of addiction at a neuronal level.
Until recently, scientists have
been limited in the technique that this disease could be observed at the
neuronal level. New research technology has enabled scientists to begin
observing the specific physical implications of addiction on specific neurons.
Specifically, optogenetics is a revolutionary tool that has enabled
neuroscientists the ability to observe neuronal activity directly.
Optogentics allows neuroscientist
to modulate specific neuronal cells and observe them in specific time and
place. This is an extremely unique techniques because of the fact that it has
such precise temporal and spatial
control. Using optogenetics, neuroscientists can excite or inhibit certain
neuron complexes, using light at specific wavelengths, in order to observe the
responses and gain further insight into the function of specific neuronal circuits.
Because of the invasive nature of this approach, optogenetics is only used on
animal subjects, but the results shed great light on similar structures in
humans. The implementation of optogenetics has provided great insight on the
affects of drugs on the brain.
Using optogenetic technology, lead
researcher Mary Kay Lobo has studied specific neurons in the nucleus accumbens,
a region of the brain that has a significant role in reward, pleasure,
aversion, and reinforcement. These researchers in her lab at Mount Sinai School
of Medicine have found 2 main neurons, D1 and D2, that play a leading role in
the cocaine reward system: “Activation of D1 neurons increase cocaine reward
whereas activation of D2 neurons decreases cocaine reward”. This type of feedback mechanism is seen in
many processes in the body, where one type stimulates a response and the other
inhibits. According to this research, addiction becomes a high risk when
exposure is increased because there is an imbalance in the state of both
neurons: D1 neurons are increases and D2 neurons are decreased.
This finding provides researchers
with the potential to create a new drug therapy that could selectively alter
the neuronal activity of D1 and D2 neurons. These developments in technology
greatly impacted the way scientists are able to observe functions in the brain.
This allows new innovations in treatments that can greatly benefit therapy
methods for addictions, as well as many other mental illnesses. While there is still much to be learned about
the psychology and neuroscience behind addiction, researchers continue to make
new strides in advancing the field.
http://www.sciencedaily.com/releases/2010/10/101018121438.htm
"Why Cocaine Is so Addictive: Activation of Specific
Neurons Linked to Alterations in Cocaine Reward." ScienceDaily.
The Mount Sinai Hospital, 18 Oct. 2010. Web. 16 Oct. 2015.
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