Reward and information are independently optimized in the human prefrontal cortex, while their signals combine in subcortical regions.

A compact neural network can form various associative memories that are encoded in a distributed manner, where each neuron stores different components of the memory.

Cortical network model suggests a mechanism explaining the link between NMDAR synaptic and spike synchrony deficits observed in a pharmacological monkey model of prefrontal network failure in schizophrenia.

The lysosomal ion channel TPC2 emerges as an example of an ion channel in which ion selectivity is not fixed but rather agonist-selective.

Cells adapt to extracellular hypertonicities using regulatory volume increase (RVI), and TNFR1-mediated NFkB activation is indispensable for RVI, but the increased cytoplasmic macromolecular crowding can inhibit TNFR1 signaling and prevent RVI at severe hypertonicities.