Claire Francesca Meehan

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

The paper discovers a new synaptic structure called the Honeycomb Synapse in the spinal cord, showing its vulnerability in ALS models.

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 study identifies synapse-specific pathology in a TDP43 mouse model of ALS, showing changes in cholinergic and excitatory synapses but not astrocytic pathology.

This study identifies intrinsic biophysical properties of gamma motoneurons in mice, revealing mechanisms underlying their low recruitment threshold and high firing rates.

This study shows that TDP-43 pathology in the TDP43-ΔNLS mouse model drives hyperexcitability in spinal motoneurones, with reversible effects upon transgene resuppression.

The paper shows that cytoplasmic TDP-43 accumulation in a mouse model leads to changes in C-bouton number and size, with sex-specific effects on motoneurones.

This study investigates age-related changes in spinal motoneurone excitability in C57BL/6J mice, finding homeostatic adjustments maintain gain control despite intrinsic property changes.

The paper investigates excitability changes in G127X SOD1 mice at symptom onset, finding increased Na+ currents and longer axon initial segments (AISs) in spinal motoneurones.

This study investigates excitability of spinal motoneurones in G93A SOD1 ALS mice and finds no deficits in repetitive firing, but increased input responsiveness and persistent inward currents.