Juan Burrone

The paper maps spatial subdomains in the zebrafish optic tectum that encode different visual features using information theory.

The paper develops U7 snRNA therapeutics to correct TDP-43-dependent mis-splicing in ALS, restoring gene expression and neuronal function in human iPSC-derived neurons.

The paper shows that increased HCN1 activity in excitatory neurons causes excessive network bursting in Dravet syndrome, suggesting HCN1 as a therapeutic target.

The paper shows that chronic inactivity does not broadly affect action potentials in neocortical neurons but does in hippocampal neurons under specific conditions.

The paper shows that in vivo modulation of network activity changes the nanoscale organization of axo-axonic synapses, reducing Gephyrin SSD volume and weakening synaptic contacts.

The paper introduces a software workflow for correlating optical and electron microscopy data to target specific regions of interest for electron tomography analysis.

This study shows that loss of TDP-43 causes synaptic dysfunction through a cryptic exon in UNC13A, which is rescued by antisense oligonucleotides.

The paper shows that excitatory and inhibitory synapses are tightly balanced along dendrites in developing hippocampal neurons, with this balance declining as the neurons mature.

This study shows that TDP-43G298S mutations in human iPSC-derived motor neurons alter axon initial segment structure and neuronal excitability at different developmental stages.

This study shows that long-term cholinergic stimulation increases the proportion of hyperadapting CA3 pyramidal neurons in hippocampal slices.

The paper identifies multi-synaptic boutons (MSBs) in CA1 hippocampal connections, which show reduced variation in synaptic properties and may support network synchrony.

The paper uses GEVIs to show that voltage-gated potassium channels maintain action potential shape fidelity in distal axons of hippocampal neurons.

This study shows that homeostatic plasticity rules govern axo-axonic synapse formation in chandelier cells, with activity changes during specific developmental windows altering synaptic connectivity.

The paper shows that apoptosis of inhibitory interneurons in the cortex is regulated by neuronal activity and can be modulated to adjust their numbers.