The vitamin A derivative, all-trans retinoic acid, induces protein-synthesis-dependent synaptic plasticity in the human brain.

Increasing cortical plasticity leads to better one-trial memory but more interference effects on semantic-like memory.

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.

Neuromodulation of the expression of Hebbian plasticity enables rapid cortical sensory-induced remodeling in post-critical period adults, and can rescue deficits induced by prolonged sensory deprivation.

Building on previous work (Kaneko and Stryker, 2014), we report that the specific population of inhibitory neurons that increases the responses of neurons in the visual cortex during locomotion will also, when activated or blocked artificially, dramatically alter adult cortical plasticity, revealing that the aerobic exercise of locomotion is not necessary.

Biochemically detailed modelling of pathways leading to post-synaptic plasticity reveals the dependence of neocortical LTP/LTD on the availability of different proteins and stimulation patterns.

Inhibitory synaptic plasticity provides a flexible and biologically plausible circuit mechanism to detect the novelty of bottom-up stimuli and to generate stimulus-specific adaptation.

Repression of the G protein-coupled chemokine receptor CCR5 enhances MAPK/CREB signaling, long-term potentiation, somatosensory cortical plasticity, and learning and memory, while CCR5 over-activation by viral proteins may contribute to HIV-associated cognitive deficits.

Accumulation of perineuronal nets around parvalbumin (PV)-positive inhibitory interneurons closes visual cortical plasticity by selectively down-regulating thalamic synapses onto PV cells in a sensory-dependent manner.

Matrix metalloproteinases play a crucial role in adult visual plasticity in the brains of healthy and stroke-affected mice and their activity has to be within a narrow window for experience-induced plasticity to occur.