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.
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.
Enhanced Gq-signaling-mediated activation of forebrain excitatory neurons in postnatal life programs enhanced anxiety-, despair- and schizophrenia-like behavior, recapitulating key aspects of the behavioral consequences of early life adversity.
Ketamine, an NMDA receptor antagonist and experimental model for schizophrenia, produces decision-making deficits in monkeys, which are predicted by a lowering of cortical excitation-inhibition balance in a spiking circuit model.
fMRI evidence for distinct hierarchical alterations in intrinsic neural timescales for different positive symptoms of schizophrenia support hierarchical perceptual-inference models of psychosis and suggest local increases in excitation-inhibition ratio.
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.