Input from the ventral hippocampus to the medial prefrontal cortex regulates social memory in wild type mice and atypically-strengthened input causes social memory dysfunction in Rett syndrome mice.
The well-established link between stress and depression could be due to the activity of a population of cells in prefrontal cortex that express a gene mutated in the rare disorder Wolfram syndrome.
A striking dissociation exists in the medial prefrontal cortex, with different brain regions responding to value when commitments are deferred to the future and when prospects are judged to be undesirable.
When the fear-enhancing effects of prior exposure to stress are absent, the expression of fear reflects normal neural activity in the medial prefrontal cortex, not stress-induced hyperactivity in the amygdala.
Establishment of two-photon imaging with a 1100-nm laser, which underfills the objective's back aperture, detects activity of multiple neurons in the prelimbic area and hippocampal CA1 region of the intact mouse brain.
Loss of REM sleep increases sucrose and fat consumption in mice; and inhibiting the prefrontal cortex reverses the increased consumption of sucrose, but not fat, following REM sleep loss.
A domain-general structure learning mechanism, supported by anterior insula, moves beyond explicit category labels and dyadic similarity as the sole inputs to social group representations and predicts ally-choice behavior.
Intergroup conflict increases human endogenous oxytocin, which predicts the medial prefrontal activity associated with ingroup pain and propensity to seek revenge upon the outgroup.
