Krishnapriya Hari

Activity-dependent structural plasticity of myelinated axons tunes their excitability

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

GABAA receptor mediated facilitation of proprioceptive afferent transmission to motoneurons is facilitated by TRPM8 channels on C-fibres that are gated by serotonin.

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.

GABAB receptors mediate presynaptic inhibition of proprioceptive afferents and have reduced action after spinal cord injury.

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

Widespread innervation of motoneurons by spinal V3 neurons globally amplifies locomotor output in mice.

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

GABA Increases Sensory Transmission In Monkeys

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

Locomotor-related propriospinal V3 neurons produce primary afferent depolarization and modulate sensory transmission to motoneurons

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

GABA facilitates spike propagation through branch points of sensory axons in the spinal cord

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

Post-activation depression produces extensor H-reflex suppression following flexor afferent conditioning

The paper investigates the mechanism of extensor H-reflex suppression by flexor afferent conditioning, finding it results from post-activation depression of Ia-afferents and long-lasting inhibition of motoneurons, not direct presynaptic inhibition.