Trajectories of adolescent drinking behavior between age 14 and 19 years can be predicted from bilateral striatal and cerebellar grey matter at 14 years of age.

Layer-specific microstructural changes contribute to the maturation of cortical organisation during adolescence.

Rat brains mature to increase metabolic connectivity between network components and establish energy efficiency in the midline structures from childhood to early adulthood.

Early life adversity led to hyper-innervation from the basolateral amygdala to the prefrontal cortex earlier in females than males and disrupted maturation of functional connectivity, which predicted anxiety-like outcomes.

The excessive behavioral variability associated with adolescence is the result of greater instability of widespread or global gain signals which produces greater variability in the amplitude of expression of whole-brain states of task-related activity.

An evolutionarily conserved mechanism involving translational control by p-eIF2α underlies vulnerability to nicotine addiction.

Mild-to-moderate sensorineural hearing loss causes changes in the neurophysiological functioning that emerge during adolescence, as suggested by both cross-sectional and longitudinal designs.

Vulnerability to cocaine addiction during adolescence depends on translational control.

Extrasynaptic GABA_A receptors that emerge at puberty trigger adolescent synaptic pruning; pruning is prevented and cognition is impaired if the receptors are absent.