Sensory deprivation suppresses cortical responsiveness through a selective remodeling of excitatory and inhibitory microcircuit motifs, by simultaneously amplifying feedforward and suppressing feedback excitation.

Excitation-inhibition imbalance affects medial prefrontal cortex differently in autistic males versus females.

The age-dependent shift of prefrontal excitation-inhibition (E-I) ratio toward inhibition causes sparser and decorrelated activity, while its impairment might relate to neurodevelopmental disorders.

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.

Delayed inhibition precisely balances excitation from arbitrary combinations of CA3 neurons and controls the gain of CA1 output by reducing inhibitory delay with increasing excitation.

Immature and mature granule cells in the hippocampal dentate gyrus show differing responses to physiologically relevant stimuli, with immature cells better at encoding stimulus frequency and mature cells better at encoding stimulus onset.

Hippocampal activity during memory recall predicts a transient increase in the ratio between neocortical glutamate and GABA, thereby allowing otherwise dormant memories to be released.

Feedforward inhibition generates motion anticipation by selectively decreasing sensitivity to a stimulus as it moves across the latter part of a retinal ganglion cell's receptive field.

The hierarchy of entorhinal grid cell modules with constant scale ratios can self-organize through a new geometrically organized attractor mechanism.

PTEN mutations disrupt inhibitory GABAergic signaling, causing neurodevelopmental defects that can be mitigated by β-hydroxybutyrate, which activates DAF-16/FOXO and may offer a therapeutic approach for excitation/inhibition imbalances.