By Donald J. Cohen, Dante Cicchetti
This quantity applies a number of degrees of study to neurobiological developmental association, and functioning in normality and psychopathology. It additionally covers issues valuable to a developmental standpoint on neuroscience.
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This quantity applies a number of degrees of study to neurobiological developmental association, and functioning in normality and psychopathology. It additionally covers subject matters valuable to a developmental point of view on neuroscience.
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Additional info for Developmental Neuroscience
2001). , 2001). However, in adolescence and adulthood, brain size of those with Autism does not differ from that of nonautisitc individuals (Aylward, Minshew, Field, Sparks, & Singh, 2002). Although the increases in brain volume are marked, the specific underlying cellular components of increased brain volumes are unknown to date. , 2003). In addition, the cause of the increase in brain volume is not completely understood, but clearly reflects some type of dysregulation in one or more stages of brain developmental processes; however, it appears that the early transient period of brain overgrowth is an important underlying factor in the emergence of many of the behavioral symptoms seen in Autism.
A growing body of investigations indicates that excitatory input plays a prominent role in the formation of many neuronal populations. In fact, in the mature central nervous system pools of progenitor cells appear to proliferate and migrate well into adulthood. For example, Kempermann, Kuhn, and Gage (1998) discovered that neurogenesis continues to occur in the dentate gyrus of senescent mice and can be stimulated when the mice are placed in an enriched environment. Kempermann et al. (1998) found that neurogenesis declined with increasing age; however, stimulation of adult and aged mice by changing from regular housing to an enriched environment that provided opportunities for social interaction, physical activity, and exploration brought about an increased number of survival cells.
As Rakic (1988a, 1988b, 1996; Sidman & Rakic, 1982) and Nowakowski (1987; Nowakowski & Hayes, 1999) have concluded, during periods of rapid brain development in which neuronal migration is occurring and synaptic connections are formed the fetal brain is especially vulnerable. , 2005), along with obstetric complications, such as perinatal hypoxia (Cannon, 1998), in concert with the genetic predisposition to Schizophrenia, may exert dramatic effects on the regions of the brain experiencing the most rapid growth.