Book contents
- Frontmatter
- Contents
- List of Contributors
- Preface
- NEURODEVELOPMENTAL MECHANISMS IN PSYCHOPATHOLOGY
- Part One Basic Mechanisms in Prenatal, Perinatal, and Postnatal Neurodevelopmental Processes and Their Associations with High-Risk Conditions and Adult Mental Disorders
- Part Two Animal Models of Neurodevelopment and Psychopathology
- Part Three Models of the Nature of Genetic and Environmental Influences on the Developmental Course of Psychopathology
- 10 Genetic Structure of Neurodevelopmental Traits: Implications for the Development (and Definition of) Psychopathology
- 11 Prospects and Problems in the Search for Genetic Influences on Neurodevelopment and Psychopathology: Application to Childhood Disruptive Disorders
- 12 Developmental Psychoneuroimmunology: The Role of Cytokine Network Activation in the Epigenesis of Developmental Psychopathology
- 13 The Hypothalamic–Pituitary–Adrenal System (HPA) and the Development of Aggressive, Antisocial, and Substance Abuse Disorders
- 14 Neuroendocrine Functioning in Maltreated Children
- 15 Toward Unraveling the Premorbid Neurodevelopmental Risk for Schizophrenia
- 16 Interactions of the Dopamine, Serotonin, and GABA Systems During Childhood and Adolescence: Influence of Stress on the Vulnerability for Psychopathology
- Part Four The Neurodevelopmental Course of Illustrative High-Risk Conditions and Mental Disorders
- Index
- References
16 - Interactions of the Dopamine, Serotonin, and GABA Systems During Childhood and Adolescence: Influence of Stress on the Vulnerability for Psychopathology
Published online by Cambridge University Press: 10 August 2009
- Frontmatter
- Contents
- List of Contributors
- Preface
- NEURODEVELOPMENTAL MECHANISMS IN PSYCHOPATHOLOGY
- Part One Basic Mechanisms in Prenatal, Perinatal, and Postnatal Neurodevelopmental Processes and Their Associations with High-Risk Conditions and Adult Mental Disorders
- Part Two Animal Models of Neurodevelopment and Psychopathology
- Part Three Models of the Nature of Genetic and Environmental Influences on the Developmental Course of Psychopathology
- 10 Genetic Structure of Neurodevelopmental Traits: Implications for the Development (and Definition of) Psychopathology
- 11 Prospects and Problems in the Search for Genetic Influences on Neurodevelopment and Psychopathology: Application to Childhood Disruptive Disorders
- 12 Developmental Psychoneuroimmunology: The Role of Cytokine Network Activation in the Epigenesis of Developmental Psychopathology
- 13 The Hypothalamic–Pituitary–Adrenal System (HPA) and the Development of Aggressive, Antisocial, and Substance Abuse Disorders
- 14 Neuroendocrine Functioning in Maltreated Children
- 15 Toward Unraveling the Premorbid Neurodevelopmental Risk for Schizophrenia
- 16 Interactions of the Dopamine, Serotonin, and GABA Systems During Childhood and Adolescence: Influence of Stress on the Vulnerability for Psychopathology
- Part Four The Neurodevelopmental Course of Illustrative High-Risk Conditions and Mental Disorders
- Index
- References
Summary
The past decade has been characterized by a significant change in the approach of psychologists and neuroscientists to the study of psychopathology (Cicchetti, 1993; Cicchetti & Cannon, 1999) and how we conceptualize the etiology of mental illness during childhood, adolescence, and adulthood (Benes, 1995). Among these disorders, schizophrenia and, more recently, bipolar disorder have received the most attention with recent postmortem studies having provided compelling evidence for a defect of GABAergic neurotransmission playing a role in its pathophysiology (for a review, see Benes & Berretta, 2001). For example, findings of a decreased density of interneurons (Benes, McSparren, Bird, SanGiovanni, & Vincent, 1991; Benes, Kwok, Vincent, & Todtenkopf, 1998), reduced GABA uptake (Simpson et al., 1989; Reynolds, Czudek, & Andrews, 1990), increased GABA receptor binding activity (Benes, Khan, Vincent, & Wickramasinghe, 1996; Benes, Vincent, Alsterberg, Bird, & SanGiovanni, 1992), decreased GABA terminals (Benes, Todtenkopf, Logiotatos, & Williams, 2000), and reduced expression of mRNA for GAD65 and GAD67 (Akbarian et al., 1995; Guidotti et al., 2000; Heckers et al., 2001; Volk, Austin, Pierri, Sampson, & Lewis, 2000) reported to date are consistent with the idea that there may be a decrease of GABAergic cells and/or activity in these disorders. Since the mechanism of action of antipsychotic medication involves blockade of both dopamine and serotonin receptors (Meltzer, 1994), a key question is how GABA cells interact with these monoaminergic systems in corticolimbic regions of schizophrenic brain.
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- Neurodevelopmental Mechanisms in Psychopathology , pp. 384 - 402Publisher: Cambridge University PressPrint publication year: 2003