The brain is an amazingly complex, still poorly understood, organ. Hundreds of billions of cells bathe one another in chemical messengers that influence moment to moment changes in brain function, behavior, and experience. Some chemical messengers can also trigger changes in gene expression in other cells, leading to long-term changes in how they look and operate, and how the individual thinks and acts. The current chemical milleu of your brain governs how you feel at this very moment -- how attentive you are, whether you are deeply satisfied with your life, whether your foot itches, you name it.
During adolescence, brain organization and function enter a unique period of flux. As an individual makes the transition from childhood to adulthood, from dependence to independence, the changes in behavior are dramatic. Not surprisingly, so are the changes in brain function that give rise to these behaviors. As we will see, the circuits that coordinate our behaviors, help us make good decisions and control our impulses, react appropriately in different situations, govern our eating and sleeping habits, etc., are being remodelled during the teen years. Much of this remodelling is influenced by an individual's interactions with the outside world, a fact that makes perfect sense given the nature of adolescence as a stage of intense personal evolution that prepares one to survive on their own outside of the nuclear family. The brain of an adolescent is highly moldable by experience, moreso than the brain of a full grown adult. The fact that people are willing to completely disrupt their lives to return to their high school reunions 50 years after they graduate is, I think, a pretty clear indication of just how important the adolescent years are for shaping who we are and how our brains function. In this section, we will explore some of the many changes taking place in the brain during the adolescent years.
Overproduction of neuronal tissue is a central theme in early brain development, from the womb to late childhood. Human infants are born with far more neurons than are present in the adult brain. The selection process that determines whether an individual cell lives or dies is based on several factors, including the transmission of neurotrophic factors from the post-synaptic cell to the pre-synaptic cell in response to excitatory synaptic activity. In this way, cells that fire together wire together, and those that do not make meaningful contacts with other cells do not survive. One key benefit of this process is that it allows a child's brain to be sculpted by his/her interactions with the outside world (Chugani, 1998).
In recent years, it has become clear that, during adolescence, as in childhood, the brain is highly plastic and shaped by experience. A substantial number of synapses are eliminated, or pruned, in the cortex during adolescence, and this process is presumably influenced, at least in part, by interactions with the outside world (Huttenlocher, 1979; Lidow et al., 1991; Seeman, 1999). It is tempting to conclude that adolescent brain development must simply be an extension of childhood brain development; that it represents a transition stage between childhood and adulthood in a manner similar to how adolescence itself has long been viewed. In actuality, it appears that many of the changes that take place during the second decade of life are novel and do not simply represent the trailing remnants of childhood plasticity.
Some of the most intriguing changes observed thus far occur in the frontal lobes, brain regions that play critical roles in memory, voluntary motor behavior, impulse control, decision-making, planning, and other higher order cognitive functions. Frontal lobe gray matter volumes, which represent dense concentrations of neuronal tissue, increase throughout childhood and do not reach their peak until roughly the age of 12, at which point they decline throughout the second decade of life. The decreased gray matter volumes appear to reflect both an elimination of synapses and an increase in myelination, a process by which glial cells surround neuronal axons and enhance the speed and distance of signal transmission. A parallel increase in overall metabolism occurs in the frontal lobes during the first decade of life and then decreases during early adolescence to reach adult levels by the age of 16-18 (Chugani, 1998). Importantly, such declines during adolescence do not reflect a diminution of frontal lobe function. Indeed, there appears to be an increased reliance on the frontal lobes in the control of behavior, a process commonly referred to as frontalization (Rubia et al., 2000). At the same time that gray matter volumes and metabolism decrease, neural activity during the performance of certain tasks becomes more focused and efficient (Casey, 1999; Rubia et al., 2000; Luna et al., 2001). Thus, it appears that adolescent brain development, at least in the frontal lobes, represents a very unique stage of change.
Additional research suggests that similar changes occur elsewhere in the cortex during adolescence. As in the frontal lobes, gray matter volumes in the parietal lobes, which are involved in processing sensory information and evaluating spatial relationships, peak at around age 11 and decrease throughout adolescence (Geidd et al., 1999). Gray matter volumes in the occipital lobes, which are dedicated to processing visual information, increase throughout adolescence and into the early 20s (Geidd et al., 1999). Gray matter volumes in the temporal lobes, which are critically involved in memory formation, as well as visual and auditory processing, do not reach maximum until the age of 16-17 (Geidd et al., 1999).
A variety of changes in subcortical structures have also been noted. For instance, the corpus collosum, a thick bundle of axons that allows the two cerebral hemispheres to communicate with one another, increases in size during adolescence (Geidd et al., 1999). Also, in the rat, levels of dopamine receptors in the nucleus accumbens increase dramatically between PD 25-40 (Teicher et al., 1995), an age range that falls within the window of periadolescent development (Spear, 2002). Dopamine receptor levels in the striatum also increase early in adolescence and then decrease significantly between adolescence and young adulthood (Teicher et al., 1995). Further, the numbers of GABAA receptors increase markedly in a variety of subcortical structures during early adolescence (PD 28-36), including the cerebellum and medial septal nucleus (Moy et al., 1998). As in the frontal lobes, age-related changes in brain activation during task performance have been observed in the cerebellum, superior colliculus, thalamus, striatum, parietal cortex, and hippocampus (Luna et al., 2001; Mueller et al., 1998).
It has become quite clear over recent years that alcohol impacts both behavior and brain function differently in adolescents and adults (Smith, 2003). For instance, the available evidence suggests that adolescents are more vulnerable than adults to the effects of alcohol on both memory and memory-related brain function, while being less vulnerable to other effects of the drug.
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