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.
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.
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.
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.
