Brain-wide activation patterns reveal the distinct and shared neurophysiological impacts of ketamine and isoflurane, highlighting key nuclei involved in the modulation of general anesthesia.

Interconnected ventral tegmental area and medial prefrontal cortex circuits causally link dopamine dynamics, aversive learning, and the effects of a promising rapidly acting antidepressant ketamine.

The rapid antidepressant actions of low dose ketamine occur through the direct relief of suppression of protein synthesis via antagonism of a subset of NMDA receptors containing the GluN2B subunit.

There is substantial individual variation in behavioral and neural responses to acute ketamine administration in healthy controls, which emphasises the need for personalized approaches when harnessing ketamine as a treatment for depression.

Ketamine induces the expression of Ca²⁺-permeable AMPA receptors to enhance synaptic glutamatergic and Ca²⁺ activity in neurons to cause rapid antidepressant effects.

Ketamine strengthens connections between two brain regions that are involved in the production and regulation of dopamine, which may explain how the drug can alleviate depression.

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.

The NMDA receptor might preferentially mediate immediate experience/impact of events with negative over positive valence.

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.