| Researched and written by ZOFIA HOCHTAUBEL
One of our archenemies is addiction, which is deeply woven within the fabric of our society. It is a deceitful force that takes many forms, whether in the grip of a substance, the charm of an action, or the enslavement of an emotion. The workings of addiction have puzzled us for centuries. Why is it that after using a cigarette once, we crave more and more?
To answer these questions, we must understand what happens in our brains when we give in to our addiction:
It's fascinating to think that if we compare memory to dependence, we will find a lot of parallels. Memories are created as a result of synaptic plasticity, which is the ability of neurons to modify the strength of synapses—connections between individual neurons. These processes are activated when we engage in addictive behaviors. So, the more we give in to our addiction, the stronger the neural connections that are connected to it get. This can eventually result in a stronger desire and craving for the addictive substance or behavior.
Furthermore, studies have demonstrated that addictive substances take over our brain's reward system by releasing a lot of dopamine, a neurotransmitter linked to pleasure. Due to this release of dopamine, a strong reinforcement loop is created that drives us to continuously seek out the addictive substance or behavior.
But what exactly is this reward system?
The reward system includes structures called the ventral tegmental area and the nucleus accumbens. In the ventral tegmental area, dopaminergic fibers forming the mesocortical pathway also send projections that end in the prefrontal cortex. The prefrontal cortex contains dopamine D1 and D2 receptors, with D1 receptors on postsynaptic membranes and D2 receptors on pre-and postsynaptic membranes. Presynaptic receptors, compared to postsynaptic ones, are characterized by up to a hundred times greater sensitivity to dopamine.
This is why D2 receptors are activated at lower dopamine concentrations than D1 receptors. Due to the ventral tegmental area's (VTA) relatively slow tonic firing of dopamine neurons that project to the cortex, the prefrontal cortex typically receives a low-level, stable flow of dopamine. Dopamine neurons, however, fire much more quickly in response to an extraordinarily rewarding event. An abrupt, but brief rise in dopamine is the result of this phasic firing, which can activate D1 receptors and is believed to be necessary for dopamine to exert its full rewarding effects. Addiction-inducing drugs, psychostimulants in particular, mimic the high levels of dopamine brought on by phasic firing and thereby trigger the D1 and D2 receptors.
Why do we suddenly feel the need to use drugs again?
Under normal circumstances, the activation of dopaminergic neurons signals the presence in the environment of factors necessary for survival, such as food and water. While eating, dopamine is only secreted for about half an hour, whereas drugs can increase its concentration for several hours. Like hot tea on a freezing day, the initial flood of this neurotransmitter seems to be very pleasant. But, when an addictive substance is consumed repeatedly, the brain starts to interpret the rise in dopamine as confirmation that the substance is essential for survival. That is why addicts feel a constant urge to satisfy their hunger.
The system in our brains that controls motivational processes changes due to addiction, and regaining the strength of synapses from before substance abuse is as challenging as going back in time and erasing memories. Teenagers and young adults are particularly vulnerable to developing substance use disorders because the parts of their brains that process risk, weigh options, and make decisions do not fully mature until they are in their mid-20s. Early adopters of illegal addictive substances frequently consume more drugs over time and are more likely to develop substance use disorders. According to research, adolescents who started smoking marijuana earlier—before the age of 16—smoked twice as often as those who started smoking later.
What about treatment?
Since addiction is a chronic disease, treatment should be based on a sustained intervention model, with the intensity of the intervention varying according to the disease's stage. Additionally, the severity of the addiction and the presence of comorbidities must be considered when tailoring the course of treatment. Animal studies using substances that are addictive have shown that it is possible to weaken synapses and rebuild the reward system.
These studies support the idea that effective therapeutic avenues for reversing addiction's debilitating effects might be developed by developing new pharmacological agents and other treatments.
Sources
“Life experiences and addictive substances change your brain in a similar way.” by Julie Kauer from the book “Think Tank” by David J. Linden
“The Neuroscience of Drug Reward and Addiction” by Nora D. Volkow, Michael Michaelides, and Ruben Baler
“Neuroscience of Addiction: Relevance to Prevention and Treatment” by Nora D. Volkow, M.D., and Maureen Boyle, Ph.D.
“The neurobiology of addiction” by George R. Uhl, George F. Koob, and Jennifer Cable
“The Impact of Initiation: Early-onset marijuana smokers demonstrate altered Stroop performance and brain activation.” K.A. Sagar, M.K. Dahlgren, and A. Gönenç, M.T. Racine, M.W. Dreman,and S.A. Grubera
Encyclopedia of Neurophysiology https://neuroexpert.org/wiki/uklad-dopaminergiczny/
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