David J. Bennett

The paper shows that activity can rapidly thin myelinated axons, increasing their excitability, and that this change is reversible and clinically relevant.

This study shows that Sall3 is essential for forming GABApre synapses on Ia afferents, and its loss disrupts motor behavior by impairing presynaptic inhibition.

The paper shows that axonal sodium currents drive doublets in motoneurons, amplifying force through nonlinear mechanisms, with neuromodulation affecting both timing and gain.

The paper shows serotonin inhibits nociceptive C-fibres and GABAergic input to proprioceptive Ia afferents, reducing motoneuron activity through TRPM8 and 5-HT1D receptor mechanisms.

This paper identifies GABAB receptors as mediators of presynaptic inhibition in Ia afferents, showing their reduced function after spinal cord injury.

The paper shows that V3 neurons in mice amplify locomotor output by increasing motoneuron excitability across all hindlimb muscles.

This study shows that GABA facilitates sensory transmission in monkeys, increasing spinal and cortical neural responses to sensory inputs.

The paper identifies propriospinal V3 neurons as the source of primary afferent depolarization (PAD) and shows their role in modulating sensory transmission to motoneurons.

The paper shows that GABAergic neurons facilitate sensory feedback by preventing spike propagation failure at axon branch points through GABAA receptor activity.

This study shows that nerve excitability test results in rat motor axons are similar whether the animals are awake or anesthetized with sodium pentobarbital.