Developmental Neuroscience in One Volume

PsycCRITIQUES ◽  
2013 ◽  
Vol 58 (45) ◽  
Author(s):  
Sheila O’Brien Quinn
2020 ◽  
Author(s):  
Adriana Sofia Méndez Leal ◽  
Jennifer A Silvers

Emotion regulation is a critical skill that promotes physical and mental health across the lifespan. This chapter describes the neural networks that underlie emotion regulation, and explores how these networks develop during childhood and adolescence. We consider two forms of emotion regulation: self-regulation and social regulation. While developmental theories suggest that parents socially regulate their children’s emotions so as to scaffold burgeoning self-regulation abilities, little neuroscience work has considered the development of self- and social regulation together. Here, we address this gap in the literature by describing what is known about the neurodevelopment of self- and social regulation of emotions separately, and by discussing how they might inform one another. Given that little developmental neuroimaging research has examined social regulation, we draw inferences from adjacent research areas including social regulation of stress physiology. Finally, we provide suggestions for future developmental neuroscience work on self and social emotion regulation.


2001 ◽  
Vol 35 (3) ◽  
pp. 272-281 ◽  
Author(s):  
Judith L. Rapoport ◽  
Xavier F. Castellanos ◽  
Nitin Gogate ◽  
Kristin Janson ◽  
Shawn Kohler ◽  
...  

Objective: The availability of non-invasive brain imaging permits the study of normal and abnormal brain development in childhood and adolescence. This paper summarizes current knowledge of brain abnormalities of two conditions, attention deficit hyperactivity disorder (ADHD) and childhood onset schizophrenia (COS), and illustrates how such findings are bringing clinical and preclinical perspectives closer together. Method: A selected review is presented of the pattern and temporal characteristics of anatomic brain magnetic resonance imaging (MRI) studies in ADHD and COS. These results are discussed in terms of candidate mechanisms suggested by studies in developmental neuroscience. Results: There are consistent, diagnostically specific patterns of brain abnormality for ADHD and COS. Attention deficit hyperactivity disorder is characterized by a slightly smaller (4%) total brain volume (both white and grey matter), less-consistent abnormalities of the basal ganglia and a striking (15%) decrease in posterior inferior cerebellar vermal volume. These changes do not progress with age. In contrast, patients with COS have smaller brain volume due to a 10% decrease in cortical grey volume. Moreover, in COS there is a progressive loss of regional grey volume particularly in frontal and temporal regions during adolescence. Conclusions: In ADHD, the developmental pattern suggests an early non-progressive ‘lesion’ involving neurotrophic factors controlling overall brain growth and selected dopamine circuits. In contrast, in COS, which shows progressive grey matter loss, various candidate processes influencing later synaptic and dendritic pruning are suggested by human post-mortem and developmental animal studies.


Development ◽  
2001 ◽  
Vol 128 (3) ◽  
pp. 417-426 ◽  
Author(s):  
W.Y. Kim ◽  
B. Fritzsch ◽  
A. Serls ◽  
L.A. Bakel ◽  
E.J. Huang ◽  
...  

A key factor in the genetically programmed development of the nervous system is the death of massive numbers of neurons. Therefore, genetic mechanisms governing cell survival are of fundamental importance to developmental neuroscience. We report that inner ear sensory neurons are dependent on a basic helix-loop-helix transcription factor called NeuroD for survival during differentiation. Mice lacking NeuroD protein exhibit no auditory evoked potentials, reflecting a profound deafness. DiI fiber staining, immunostaining and cell death assays reveal that the deafness is due to the failure of inner ear sensory neuron survival during development. The affected inner ear sensory neurons fail to express neurotrophin receptors, TrkB and TrkC, suggesting that the ability of NeuroD to support neuronal survival may be directly mediated through regulation of responsiveness to the neurotrophins.


Sign in / Sign up

Export Citation Format

Share Document