Resting-state MEG-activity and MRS-GABA/Glx measurements reveal that there is a significant shift in excitability during the course of schizophrenia, involving hyperexcitability during the onset and a reduction at chronic stages.

A genetic program controlling brain genes across the lifespan specifies a calendar of changes in cells, synapses and behavioural genes thereby timing the onset of mental illnesses which arise in young adults.

Genetic rescue experiments reveal that γ-secretase enzymes containing Aph1b subunits control signalling by type III neuregulin 1, with implications for schizophrenia.

Local cortical sleep features arise subcortically due to heterogeneous burst discharge in neurons of a sleep rhythm pacemaker previously thought to act uniformly.

Autistic traits are associated with weaker influence of prior expectations in visual perception, which is due to more precise sensory representations.

Parvalbumin-containing inhibitory neurons are crucial for expression of plasticity in adult visual cortex that supports visual recognition memory, but not for expression of ocular dominance plasticity that results from monocular deprivation.

The conditional reduction of glutaminase in mouse dopamine neurons selectively attenuates glutamate cotransmission at phasic frequencies, revealing the role of dopamine neuron glutamate cotransmission in the attribution of motivational salience.

Mice that lack the autism- and schizophrenia-linked gene MEF2C in cortical neurons have an imbalance of excitatory and inhibitory synapses, and impaired social and cognitive abilities.

Truncated Disrupted-in-schizophrenia 1 (Disc 1) ablates signaling of parvalbumin-expressing interneurons in the prefrontal cortex and underlies depression-related behaviour in mice.

An internal clock based on brain levels of dopamine works with the circadian clock to maintain daily patterns of alertness and activity, and may be implicated in the altered behavioral patterns seen in schizophrenia and bipolar disorder.