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.

An individualized cross-frequency coupling approach identified slow oscillation-spindle coupling strength as a novel mechanism that mediates memory formation during cortical maturation.

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.

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

Early life adversity (ELA) accelerated PV+ interneuron development in BLA and delayed the ability of pre-adolescent mice to express, but not form, an auditory conditioned fear memory in childhood.

Problematic design features in the stop-signal task for the massive Adolescent Brain Cognitive Development (ABCD) study undermine analyses of the shared data, but can be mitigated with proposed solutions.

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.

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.