Monica A. Gorassini

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 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 investigates how altered spinal motoneuron properties contribute to motor deficits in a rabbit hypoxia-ischemia model of cerebral palsy, finding significant physiological differences between affected and unaffected groups.