However, others suggest that the available synaptic storage pool is increased in adolescence relative to both child years and adulthood (Andersen, Dumont, & Teicher, 1997;Stamford, 1989). across developmental groups. Implications for the understanding of adolescent behavioral development are discussed. Keywords:Dopamine, COMT, Brain Development, Adolescence, Working Memory == Introduction == Adolescence is usually a transitional period between child years and adulthood characterized by behavioral, hormonal, and neurochemical changes designed to prepare organisms for independent survival (Casey et al., 2008;Doremus-Fitzwater et al., 2010;Spear, 2003). Although these transitions are largely positive, adolescence can be conceptualized as a period of vulnerability. Risk-taking increases during this time (Steinberg, 2008), as does vulnerability to psychiatric disorders (Kessler et al., 2005;Paus, Keshaven & Giedd, 2008). Theories abound to explain these patterns, most of which suggest that adolescent behavior patterns are attributable to changes in brain maturation during this period of the lifespan (Casey et al., 2008;Fareri et al., 2008;Steinberg, 2008). Many frameworks focus on one of two neural substrates, considering one or both. These include (a) the prefrontal cortex (PFC), which is usually structurally and functionally under-developed, leading to deficiencies in behavioral regulation, as well as (b) limbic and striatal structures, which may be characterized by relatively heightened patterns of activation, conferring a state of motivational over-drive. Simplistically put, it is hypothesized that go signals are strong, while regulatory quit or monitoring signals are Azathramycin poor. These processes may be inter-related in that sub-cortical signaling can be excessive due to a lack of overarching cortical control. Accordingly, it is unknown whether adolescents behavior patterns are due to deficiencies in the PFCs structural and functional maturation, to a subcortical system that is in over-drive and could not be Azathramycin controlled Rabbit Polyclonal to PKC delta (phospho-Ser645) even in the presence of an properly functioning PFC, or to some combination of both factors. It should also be pointed out at the outset that not all models adhere to the formulation that motivational circuits are in a state of over-drive; some propose that the opposite is Azathramycin true (Comings & Bloom, 2000;Volkow et al., 2007). Although the brain is undergoing structural refinement during adolescence, adolescents difficulties with behavioral regulation may be exacerbated by other neurodynamic processes. We have offered a unifying account of adolescent behavior that explains it in terms of the development of the dopamine (DA) system (Wahlstrom et al., 2010). Briefly, our perspective builds upon the theory that DA Azathramycin underlies a behavioral activation system that modulates incentive-motivated approach behavior (Depue Azathramycin & Collins, 1999). This system promotes reward-seeking through activity in limbic, striatal, and frontal networks, facilitating an individuals ability to translate positive motivations into adaptive actions. The adaptive pursuit of positive incentives is critical to impartial future-directed behavior. Our perspective is usually that activity in this system increases during adolescence to meet the demands associated with the transition to impartial living. The increase occurs via a tonic increase in DA availability and impacts both subcortical (limbic and striatal) and cortical (prefrontal) circuits. Operating within the context of continued structural brain development, heightened DA activity within this system may result in an apparent over-activation of incentive motivation in the absence of reliable levels of behavioral control. Regrettably, the assessment of neurochemistry in human adolescents has confirmed elusive due to methodological limitations and human subjects concerns. The purpose of the current evaluate is to describe developmental changes in the DA system through adolescence and to suggest a genetic model for how the integrity of the system can be assessed non-invasively in healthy adolescents. In addressing this aim, we will (i) provide an overview of brain development during adolescence; (ii) provide a brief overview of the DA system from a neurophysiological perspective, (iii) review the development of the DA system, presenting data from the animal literature; this evaluate represents the major portion of this paper and is intended to provide a rationale for why this system should be scrutinized in humans for its role in adolescent behavior; finally, we will (iv) present a molecular genetic strategy for the indirect assessment of human neurochemical development. We have chosen DA, the COMT Val158Met single nucleotide polymorphism, and working.