Behavioral, pharmacological, optogenetic, electrophysiological and computational analyses suggest that the anterior dorsal striatum is a causal node in the network responsible for evidence accumulation.
Cognitive reconstitution after pharmacologic unconsciousness is an extended process, executive function is more robust than expected, and the healthy human brain is resilient to the effects of deep general anesthesia.
Defects in synapse regeneration limit functional circuit recovery after nerve injury by misdirecting information via ectopic dendritic synapses, and also by functional and molecular deficits in reformed axonal synapses.
Brain recovery after injury can be predicted based on its activity and structure, which may allow us to understand why some brain injuries lead to permanent loss of cognitive function, while others do not.
A model of pathogen co-evolving with host population continuously acquiring immunity is used to identify evolutionary parameters allowing pathogen population to persist without going extinct or splitting into independent lineages.