Reactive oxygen species, previously considered damaging agents linked to pathology, are required for normal neuronal plasticity, including adjustment of synaptic terminal size, maintenance of synaptic physiology and adaptive behavioural responses.

Structural and functional striatal synaptic plasticity abnormalities occur early in a sensitive developmental period, representing a potential unique endophenotypic traits that increase the risk of manifesting clinical symptoms in DYT1 mutation carriers.

Neurons in the hypothalamus that promote satiety manifest plasticity of their response to the excitatory transmitter, glutamate, by re-organizing the composition of a specific glutamare receptor.

A novel form of hippocampal synaptic plasticity is expressed by a change in channel function of GluA3-containing AMPA-receptors.

A screen of visual-experience induced changes in newly-synthesized proteins in Xenopus optic tectum identifies unexpected candidate plasticity proteins.

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.

Evolutionary novelty is promoted by a macroevolutionary pulse of developmental plasticity, but is enhanced by secondary fixation, which permits developmental character release and further morphological exploration.

A critical regulator of inhibitory neurotransmitter signaling in the hippocampus has been identified in experiments on mice and been shown to play essential role in synaptic plasticity and memory.

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.

Genetic and electrophysiology experiments provide the first direct evidence that protein kinase C is a calcium-sensing protein in post-tetanic potentiation, a form of synaptic plasticity that supports short-term memory.