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Although extremely early and late maturation may be risk factors in development, we have seen that the overall effects of early or late maturation often are not great. Not all early maturers will date, smoke, and drink, and not all late maturers will have difficulty in peer relations. In some instances, the effects of an adolescent’s grade in school are stronger than maturational timing (Petersen & Crockett, 1985). Because the adolescent’s social world is organized by grade rather than physical development, this finding is not surprising. However, that does not mean that age of maturation has no influence on development. Rather, we need to evaluate puberty’s effects within the larger framework of interacting biological, cognitive, and socioemotional contexts (Brooks-Gunn, 1992; Sarigiani & Petersen, 2000). Pubertal Timing and Health Care What can be done to identify early and late maturers who are at risk for health problems? Adolescents whose development is extremely early or late, such as a boy who has not had a growth spurt by age 16 or a girl who has not menstruated by age 15, are likely to come to the attention of a physician. Girls and boys who are early or late maturers, but are still well within the normal range, are less likely to be seen by a physician. Nonetheless, these boys and girls may have doubts and fears about being normal that they will not raise unless a physician, counselor, or other health-care provider does. A brief discussion of the usual sequence and timing of events, and the large individual variations in them, may be all that is required to reassure many adolescents who are maturing very early or late. Health-care providers may want to discuss an adolescent’s early or late development with parents as well. Information about peer pressures can be helpful, especially the peer pressures to date on early-maturing girls and engage in adultlike behavior. For girls and boys who are in the midst of puberty, the transition to middle school, junior high school, or high school may be more stressful (Brooks-Gunn, 1988). If pubertal development is extremely late, a physician may recommend hormonal treatment. This approach may or may not be helpful (Carroll & others, 2004; Fenichel, 2004; Lee, 2003; Leschek & others, 2004). In one study of extended pubertal delay in boys, hormonal treatment helped to increase height, dating interest, and peer relations in several boys but brought little or no improvement in other boys (Lewis, Money, & Bobrow, 1977). In sum, most early- and late-maturing individuals manage to weather puberty’s challenges and stresses. For those who do not, discussions with sensitive and knowledgeable health-care providers and parents can improve the adolescent’s coping abilities (Phillips, 2003). 1 Review and Reflect ● LEARNING GOAL 1 Discuss the determinants, characteristics, and timing of puberty Review • What are puberty’s main determinants? • What characterizes the growth spurt in puberty? • How does sexual maturation develop in puberty? • What are some secular trends in puberty? • How are psychological dimensions linked to pubertal change? • What are some aspects of pubertal timing and health care? Reflect • Did you experience puberty early, late, or on time? How do you think the timing of puberty affected your development? Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Body image score +.30 +.20 +.10 Mean –.10 –.20 –.30 Puberty 77 Early development Late development Grade 6 Grade 10 FIGURE 3.8 Early- and Late-Maturing Adolescent Girls’ Perceptions of Body Image in Early and Late Adolescence
78 Chapter 3 Puberty and Biological Foundations 2 THE BRAIN (a) Incoming information To next neuron neurons Nerve cells, which are the nervous system’s basic units. Neurons Brain Structure Experience and Plasticity Axon (b) Outgoing information Cell body Nucleus Dendrites (c) Myelin sheath (d) Terminal button FIGURE 3.9 The Neuron. (a) The dendrites of the cell body receive information from other neurons, muscles, or glands. (b) An axon transmits information away from the cell body. (c) A myelin sheath covers most axons and speeds information transmission. (d) As the axon ends, it branches out into terminal buttons. www.mhhe.com/santrocka11 Neural Processes Neuroimaging Internet Neuroscience Resources Until recently, little research has been conducted on developmental changes in the brain during adolescence. While research in this area is still in its infancy, an increasing number of studies are under way (Walker, 2002). Scientists now believe that the adolescent’s brain is different from the child’s brain, and that in adolescence the brain is still growing (Keating, 2004). Neurons Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Neurons, or nerve cells, are the nervous system’s basic units. A neuron has three basic parts: the cell body, dendrites, and axon (see figure 3.9). The dendrite is the receiving part of the neuron, while the axon carries information away from the cell body to other cells. A myelin sheath, or a layer of fat cells, encases most axons. The sheath helps to insulate the axon and speeds up the transmission of nerve impulses. Interestingly, researchers have found that cell bodies and dendrites do not change much during adolescence, but that axons continue to develop (Pfefferbaum & others, 1994; Rajapakse & others, 1996). The growth of axons is likely due to increased myelination (Giedd, 1998). Researchers have found that dendritic growth can continue even in older adults, however, so further research may show more growth in dendrites during adolescence than these early studies suggest (Coleman, 1986). In addition to dendritic spreading and the encasement of axons through myelination, another important aspect of the brain’s development is the dramatic increase in connections between neurons, a process that is called synaptogenesis (Ramey & Ramey, 2000). Synapses are gaps between neurons, where connections between the axon and dendrites take place. Synaptogenesis begins in infancy and continues through adolescence. Researchers have discovered that nearly twice as many synaptic connections are made than will ever be used (Huttenlocher & others, 1991; Huttenlocher & Dabholkar, 1997). The connections that are used are strengthened and survive, while the unused ones are replaced by other pathways or disappear. That is, in the language of neuroscience, these connections will be “pruned.” Figure 3.10 vividly illustrates the dramatic growth and later pruning of synapses in the visual, auditory, and prefrontal cortex of the brain (Huttenlocher & Dabholkar, 1997). These areas are critical for higher-order cognitive functioning such as learning, memory, and reasoning. As shown in figure 3.10, the time course for synaptic “blooming and pruning” varies considerably by brain region. In the visual cortex, the peak of synaptic overproduction takes place at about the fourth postnatal month, followed by a gradual reduction until the middle to end of the preschool years (Huttenlocher & Dabholkar, 1997). In the auditory and prefrontal cortex, which are involved in hearing and language, synaptic production follows a similar although somewhat later course. In the prefrontal cortex (where higher-level thinking and self-regulation occur), the peak of overproduction takes place at about 1 year of age. Not until middle to late adolescence does this area reach its adult density of synapses. What determines the timing and course of synaptic “blooming” and “pruning”? Both heredity and experience are thought to be influential (Greenough, 2000; Greenough & Black, 1992). For instance, the amount of visual and auditory stimulation a child receives could speed up or delay the process. With the onset of puberty, the levels of neurotransmitters—chemicals that carry information across the synaptic gap between one neuron and the next—change. For example, an increase in the neurotransmitter dopamine occurs in both the prefrontal cortex and the limbic system (Lewis, 1997). Increases in dopamine have been linked
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