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

Combined pre- and postsynaptically expressed long-term plasticity of neuronal connections improves sensory discrimination, and enables rapid relearning of previously encountered information.

Temporal continuity-induced plasticity in individual neurons of inferior temporal cortex builds neural representations that underlie robust core object recognition behavior.

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.

Artificial evolution discovers biophysically plausible plasticity rules for spiking networks that perform competitively with and even outperform labor-intensive human-designed models in various learning scenarios, while providing new views on experimental data.

Combining GABA with fMRI measurements in the human brain uncovers distinct suppression mechanisms that optimize perceptual decisions through learning and experience-dependent plasticity in the visual cortex.

Dendritic calcium spikes translocate hippocampal place fields by inducing a non-Hebbian form of bidirectional synaptic plasticity that operates over a seconds-long timescale called behavioral timescale synaptic plasticity.

A comprehensive modeling approach reconciles experimental observations with classic plasticity mechanisms in the cerebellar cortex, demonstrating how learning-related changes in neural activity can appear to contradict the sign of the underlying plasticity when feedback is present.

Presynaptic plasticity in simulated neural networks with a simple biologically plausible learning rule improves metabolic efficiency and lifelong learning capabilities.

A brain-wide neuromodulatory system enables rapid cortical plasticity to occur by signaling sensorimotor prediction errors across wide regions of the cerebral cortex.