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.

Serotonin neurons in chronically isolated mice become less responsive to excitatory stimulation, but inhibiting a distinctive calcium-activated potassium channel can restore both neuronal activity and behavior.

The orphan receptor GPR158 is highly regulated by stress exposure and acts on key neuronal signaling pathways in the prefrontal cortex to control depressive-like behaviors.

Behavioral and molecular mechanistic studies elaborate the important role of ErbB4 in noradrenergic neurons associated with mania pathogenesis.

Gut microbiota can influence mPFC transcriptional profiles and myelin content, overriding the impact of genetic background in the development of social avoidance behavior.

Insulin-like growth factor-1 activates the prefrontal cortex and improves the extinction of aversive memories.

In mouse brain slices, native delta glutamate receptors carry ionic current and underlie the α1-adrenergic receptor-mediated depolarization of dorsal raphe neurons that drives action potential firing in vivo.

HCN2 channels in the ventral tegmental area play an important role in the pathophysiology of chronic mild stress-induced behavioral deficits.

Truncated Disrupted-in-schizophrenia 1 (Disc 1) ablates signaling of parvalbumin-expressing interneurons in the prefrontal cortex and underlies depression-related behaviour in mice.

¹H-Magnetic resonance spectroscopy at 14T reveals a metabolic signature for anti-depressant-like effects of acetyl-L-carnitine in nucleus accumbens of susceptible mouse.