Changes in the brain during adolescence causing addiction and fearful behaviors

Adolescence is the time period of growth and development between childhood and adulthood. Many adolescents face difficulty during this maturation period and are troubled by stressful development. This is a phase where most individuals feel an emotional disconnect with their family with an attitude screaming “I’ve got this, leave me alone!”. During the puberty period, most adolescents are thoughtless and distracted due to the surge of hormones leading to changes in behaviour which is very commonly associated with risk taking [1].  This can be an exciting as well as a critical period in an individual’s life as it is associated with various cognitive and psychological changes that promote vulnerability to fearful or anxiety related behaviours and addiction behaviours [2,3].

Fear is generally perceived as an aversive feeling and hence the individual experiencing it will exhibit a natural desire to “turn it off”. However, in adolescence, fear can also be perceived as an exciting or thrilling feeling which is attractive. For example, watching a horror movie or riding a roller coaster can provide that adrenaline rush and make these activities desirable [4]. Risky behaviour that can be otherwise considered harmful, like smoking, binge drinking or criminal behaviour increases during adolescence and can increase the morbidity in these individuals [4]. Hence, it is important to understand the neurobiological circuits involved in mediating these changes.

The neurobiology behind risky behavior

Studies performed in rodents and humans have characterized the brain of an adolescent based on functioning of two main neurological systems. One of them is the early developing “hot” system and the other one is a relatively “cold” and slowly developing system [5]. The hot system is an affective motivational system that involves the area of the brain called the “subcortical” brain region and develops early during puberty. This region is rich in the motivational hormone called “dopamine” and is associated with representation of rewards. These rewards can be anything ranging from candies, X-box, or a new car. On the other hand, the other “cold” system is associated with brain regions of the “pre-frontal cortex” which helps in self-control, planning, working memory and this region can help the individual avoid the temporary temptations to get long-term benefits. This controlling system develops during the later phase of turning into a young adult [5].

Knotch and colleagues show that the lateral area of the prefrontal cortex is likely to be involved in self-control while making a risky choice as they observed that when this particular brain region was disrupted in adults, a high amount of impulsivity and impatience was observed [6,7]. This implies that the development of this region during adolescence plays a role in such risk-taking behaviours.

Other changes associated with the developmental process between childhood and adulthood are the changes in “dopamine-receptor” densities. A receptor is the molecule to which dopamine binds to mediate a response. Studies have also shown that there is increased amounts of activity in the “striatum” region of the brain when the adolescents are anticipating or representing rewards. This implies that it would be difficult for the adolescents to stop the approach behaviour or “say no” to the cues of rewards when compared to adults or children [8,9]. Hence, it is assumed that in the adolescence phase, the decision-making processes are disrupted by an imbalance between motivational and controlling neurobiological circuits of the brain. For example, an adolescent male, when given the temptation of getting a reward of 1000 dollars by winning a dangerous street fight, would most likely do it putting them at a risk of injuring themselves. Whereas an adult would be able to make more rational decisions in such situations.

The neurobiology behind fearful behavior

Fear that is not excitatory is also observed in adolescence with the presentation of anxiety symptoms as well [3]. About 75% of people suffering with fear or anxiety disorders are reported to be adolescents [3, 10] Fear learning and regulation occurs throughout the developmental process from childhood to adulthood. Apart from the prefrontal cortex, other brain structures known as the “amygdala” and the “hippocampus” are also implicated in the regulation of anxiety and fear as these three structures are all interconnected and are a part of the brain system called “corticolimbic system.”

The amygdala is shown to play an important role in the regulation of fear learning acquisition, expression of fear and also extinction of fear. A study performed by Akirav shows that this brain region responds to various types of fear stimuli such as facial expressions, emotional stimuli or even pharmacological fear induction [11]. The amygdala can be further divided into various other regions out of which the region called the “central nucleus” is responsible for expression or output of the fear response. So, that little heart freeze you get when you almost drop your phone or that increased heart rate before a presentation is caused by the central nucleus which connects to another region called the “hypothalamus” to produce these responses [3, 12].

The hippocampus region, on the other hand, is implied in acquiring and storing the contextual fear memory. This region processes previous experiences of fear and provides information about threat or safety in various situations [12].

The neurobiology behind addiction behavior

Drug and alcohol use is also a part of the adolescence phase. The neurobiology underlying the addiction process involves dopamine as well. Dopamine action is mediated by formation of new connections in the brain and loss of the older brain connections. This leads to structural changes in the brain [13]. As mentioned above, the dopamine action occurs mainly in the striatum which is responsible to perceive rewards. However, there are other targets of dopamine action as well including the amygdala, the hippocampus and the prefrontal cortex, showing that all these circuits are interconnected. Drug or alcohol use has been associated with reduced cognitive control. The ventral area of the striatum called the “nucleus accumbens” is very commonly implicated and studied in the addiction disorders [13]. In response to drugs, dopamine flows very specifically from the “ventral tegmental area” to the nucleus accumbens of the brain. It is assumed that the increased secretion of dopamine in this pathway causes increased drug or alcohol seeking behavior.

As time passes, the addiction grows, and this addiction is a result of the switch from ventral striatum activity to dorsal striatum activity. This means that the impulsive drug seeking changes to compulsive addiction when this shift of activity occurs [14]. The region involved in self-control is also modified by drugs and alcohol. This is the “dorsolateral” prefrontal cortex which is highly activated in the early stages of addiction. Volkow and colleagues have shown that this region, over the course of addiction becomes dysfunctional, implying that the people with addiction disorders have less self-control and reasoning power [15].

This leads us to thinking that modifying the neural circuits involved in mediating fear and addiction can help in regulating or reversing the responses.

Modifying fearful and addiction behavior

Fear-based and addiction disorders can be modulated using a process called cognitive behavioural therapy (CBT). Aiding fear-based or anxiety disorders involves the use of something called “extinction learning.” This means that the individuals are subjected to repeated exposures of the fear stimuli which eventually leads to extinction of fear and desensitisation of the stimuli that causes fear or anxiety [16]. CBT is also used for the treatment of addiction through the enhancement of cognitive control. Cognitive therapies like CBT change the neurological circuitry of the brain involved in motivation and control [17].  This therapy works by regulating rational thinking which ultimately leads to regulation of negative emotions and emotional response [17]. In anxiety related disorders, CBT causes reduction in the activity in the subcortical region involving amygdala and hippocampus (amygdohippocampal subcortical region) which is implied in emotion processing. On the other hand, there is higher activation of the “frontal cortical regions” which are responsible for higher-order cognitive functions [17]. In addiction behaviours, CBT works in the same way by promoting effective decision-making. Studies have shown that the subcortical region is altered leading to higher cortical control in the individual causing increased self-control over motivational drives [18].

This brings us to the conclusion that adolescence is a phase where individuals are more prone to developing disorders of fear, anxiety and addiction. This occurs as a result of the changes in the neural circuitry as a part of the developmental process of turning into an adult. Even though therapies like CBT are available, 80% teens and adolescents suffer from anxiety disorders and do not get diagnosed [19]. Also, about 1.7 million adolescents suffer from addiction disorders involving drugs and alcohol [20]. Hence, it is important to study the neural circuitries involved in development of these disorders so that we can prevent them from carrying on to adulthood. As adolescence is a very vulnerable age, it is important to modulate the neurobiology of the circuitries in this age and address the issues of adolescents with these disorders rather than casting them out as “rebellious kids”.

References:

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