Untitled

22 BIOLOGICAL AND SOCIAL UNIVERSALSlaboratory animals as well, various examples of alleviation or emergence of symptomatologyduring adolescence have been observed. For instance, an adolescentassociateddecline in outcome following early orbital frontal lesions in Rhesusmonkeys contrasts with evidence for the emergence of more pronounced effects ofdorsolateral lesions of the PFC (Rhesus monkeys: Goldman, 1971; rats: Flores etal., 1996) or ventral hippocampus (Lipska & Weinberger, 1993) as animals reachmaturity.A number of factors may contribute to the delayed emergence or decline insymptomatology during the adolescent period. In some instances, manifestationof some early appearing deficits may decline developmentally as the brain is restructuredand refined to permit the emergence of functional compensations forthose deficits. Conversely, impaired neural regions may not become functionallymature until adolescence, and hence consequences of damage to that region maynot surface until that time. It is also possible that the sculpting of adolescent brainmay unveil early developmental compromises, plasticity-induced concessions thatmay effectively have masked adverse consequences of suboptimal genetic expressionand environmental conditions early in life.One potential contributor to the later unmaking of early neural compensationsis stress. Increased sensitivity to stressors and environmental demands has beenobserved in studies in laboratory animals following a variety of early developmentalperturbations, including perinatal stress (Cabib et al., 1993; Takahishi et al.,1992; Weinstock, 1997) and prenatal exposure to drugs including cocaine, ethanol,or diazepam (Kellogg, 1991; Mayes et al., 1998; Riley, 1990; Spear et al.,1998). Such stressor vulnerability may be particularly pronounced during adolescence,given evidence discussed earlier that this developmental transition maybe unusually stressful for the adolescent.Over the past decade there has been increasing recognition that highly conservedneural alterations during adolescence may contribute to cognitive and behavioralfunction of adolescents, their sensitivity to environmental demands, and the emergenceof psychopathology among the most vulnerable. With the increasing focuson research during adolescence and ongoing improvements in MRI technology,continued rapid progress in this area is likely, progress that will be critical fordesigning strategies to enable adolescents to meet environment challenges, channeltheir proclivities, and conquer this developmental transition while avoidinglong-term cost to themselves.ReferencesAcheson, S. K., Stein, R. M., & Swartzwelder, H. S. (1998). Impairment of semantic andfigural memory by acute ethanol: Age-dependent effects. Alcoholism: Clinical and ExperimentalResearch, 22(7), 1437–1442.