The neurobiology of adolescence: Changes in brain architecture, functional dynamics, and behavioral tendencies

Abstract

Adolescence is a period of increased behavioral and psychiatric vulnerabilities. It is also a time of dramatic structural and functional neurodevelopment. In recent years studies have examined the precise nature of these brain and behavioral changes, and several hypotheses link them together. In this review we discuss this research and recent electrophysiological data from behaving rats that demonstrate reduced neuronal coordination and processing efficiency in adolescents. A more comprehensive understanding of these processes will further our knowledge of adolescent behavioral vulnerabilities and the pathophysiology of mental illnesses that manifest during this period.

Introduction

Adolescence is a period in which individuals observe physical changes to their bodies, experience new interests and desires, and find themselves with greater freedom, independence, and responsibility. Although variably defined, adolescence is generally considered to begin with the onset of puberty and ends as one takes on adult social roles (Dahl, 2004, Spear, 2000). The span of puberty—which involves increased growth, changes in body composition, the development of gonads and secondary sexual organs and characteristics, and cardiovascular and respiratory changes—typically occurs from age 10–17 in girls and 12–18 in boys (Falkner and Tanner, 1986). As this occurs the adolescent undergoes a variety of cognitive, behavioral, and psychosocial transitions. The various changes of adolescence do not all start and end together, and thus the puzzle of relating adolescent brain changes with behavior is challenging. Studying adolescence is like shooting at a moving target, with researchers designating “adolescent” groups of different ages and levels of development. Furthermore, from the mid-19th through the 20th century, an earlier average age of menarche has been observed in the western world (Falkner and Tanner, 1986, Tanner, 1990). The educational process is more prolonged and individuals are tending to wait longer before starting their careers, getting married, and having children (Dahl, 2004). Thus, the length of adolescence is not fixed (and has been lengthening) and while the period correlates with many biological developmental processes, it is partially defined according to psychosocial and behavioral criteria. With these caveats in mind, the literature reviewed here has primarily defined adolescence in humans as the second decade of life, in monkeys as age two to four years, and in rodents as week four to week six or seven.

Despite the definitional ambiguities, it is well recognized that during this period major transitions do occur, including a variety of characteristic behavioral changes seen across species. There is increased social behavior (Csikszentmihalyi et al., 1977), novelty and sensation seeking (Adriani et al., 1998, Stansfield and Kirstein, 2006, Stansfield et al., 2004), tendencies toward risk taking (Spear, 2000, Steinberg, 2008), emotional instability (Steinberg, 2005), and impulsivity (Adriani and Laviola, 2003, Chambers et al., 2003, Fairbanks et al., 2001, Vaidya et al., 2004). Peer relationships become dominant, and there are greater inclinations to seek out fun and exciting experiences (Nelson et al., 2005). Increased novelty and sensation seeking may be evolutionarily adaptive, as these behaviors could improve the increasingly independent adolescent's chances of finding food and a mate (Spear, 2010). In modern society, however, these features can be associated with taking unnecessary risks. Therefore, adolescence is considered a period of behavioral vulnerability: teens are more likely to experiment with tobacco and illicit drugs and alcohol; drive recklessly; engage in unprotected sex; and have interpersonal conflicts (Arnett, 1992, Arnett, 1999, Chambers et al., 2003, Spear, 2000). Adolescent risk taking is more likely to occur in groups (e.g., vehicular accidents), when certain behaviors are perceived to be acceptable by one's peers (e.g., unprotected sex, drug use) (Steinberg, 2008), and in emotionally charged situations (Figner et al., 2009). Thus, while adolescents have survived the potential health problems of early childhood their morbidity and mortality rates are twice that of pre-pubescent children (Dahl, 2004).

In addition to the added risks of normal adolescent development, it is also the time when symptoms of a variety of mental illnesses often manifest, including mood disorders, eating disorders, and schizophrenia (Paus et al., 2008, Pine, 2002, Sisk and Zehr, 2005, Volkmar, 1996). During this period there is a vast array of neurobiological changes that drive everything from a cascade of hormonal signals that initiate puberty (Sisk and Zehr, 2005), to increased cognitive ability and motivational changes (Doremus-Fitzwater et al., 2009, Luna et al., 2004). Understanding precisely how the brain develops through adolescence, and relating such changes to both normal behavioral tendencies and pathological conditions, is critically important to public health. Here we review some of the behavioral, and neurodevelopmental changes of adolescence and discuss several models that connect them, including our own hypothesis of reduced processing efficiency.