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.
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.
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.
Genetic rescue experiments reveal that γ-secretase enzymes containing Aph1b subunits control signalling by type III neuregulin 1, with implications for schizophrenia.
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.
Local cortical sleep features arise subcortically due to heterogeneous burst discharge in neurons of a sleep rhythm pacemaker previously thought to act uniformly.
Striatal dopamine 2/3 receptor (D2/3R) availability is related to working memory-induced functional connectivity changes in the default mode network, and this mediates the relationship between D2/3Rs and task performance.
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.
