Synaptic zinc is a novel modulator of cortical sound processing - a modulator that increases the gain of principal neurons, but reduces the gain of interneurons.

Combined TMS-EEG can be used to further elucidate the mechanisms for pain perception and to discover biomarkers for the development of chronic pain.

Alterations to brain network communication leading to a progressive loss in descending inhibitory modulation of the spinal cord is a key determinate of pain state development following peripheral nerve injury.

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.

An epilepsy-associated potassium channel variant causes neuron-type-dependent alterations in ionic currents, neuronal excitability, and network connectivity.

Both hand and face representations remain relatively stable after arm amputation in adulthood, with no link to phantom limb pain, whereas pre-natal limb loss triggers complex patterns of remapping that do not relate to cortical topography.

Dynamic regulation of feedforward inhibition from parvalbumin-expressing inhibitory neurons is linked to the gradual restoration of cortical sensory processing following auditory nerve damage.

Cortices from 11 primate species share the same archetypal fractal shape, indicating a universal mechanism for primate and mammalian cortical folding, and suggesting novel shape biomarkers for brains.

Widespread somatosensory cortical activation following a single localised skin breaking procedure indicates a diffuse pain map in the human infant brain.

The glycinergic neurons of the cerebellar nuclei project extensively to the cerebellar cortex and inhibit GABAergic Golgi cells.