Michael Alan Cousin

This paper shows that presynaptic filopodia, driven by activity, calcium, and actin, physically modulate membrane mechanics to enhance synchronous neurotransmission and contribute to seizure generation.

This study shows that Fmr1 knockout rats exhibit early Kv7 channel dysfunction in CA1 neurons due to altered axon initial segment development, which recovers by adulthood.

This study shows TDP-43 filaments accumulate at synapses, causing presynaptic dysfunction and neuronal hyperexcitability in neurodegenerative diseases.

The paper identifies a common depression in activity-dependent bulk endocytosis across rodent models of autism spectrum disorders, suggesting it as a homeostatic response to hyperexcitability.

The paper introduces NbLumSyt1 nanobinders for analyzing synaptic vesicle dynamics in rodent and human models with improved precision and versatility.

This study identifies the phosphorylation-dependent interaction between Amph1 and endophilin A1 as essential for synaptic vesicle endocytosis.

This paper shows that botulinum neurotoxin type A (BoNT/A) toxicity relies on synaptotagmin 1 (Syt1), which forms nanoclusters with PSG and SV2 on neuronal membranes, enabling endocytic targeting and neuronal communication disruption.

This study shows that a mutation in DNM1 causes epilepsy by disrupting synaptic vesicle endocytosis, and that a drug can reverse these effects in a mouse model.

This study shows that CDKL5 deficiency impairs synaptic vesicle endocytosis in neurons, highlighting its presynaptic role in epilepsy.

The paper shows that SV2A-Syt1 nanoclusters limit dynamin-1 recruitment, thereby controlling the re-entry of Syt1 into recycling synaptic vesicles.

The paper shows that Dynamin 1xA forms molecular condensates with Syndapin 1 at endocytic sites, enabling ultrafast endocytosis by bypassing the recruitment step.

The paper shows that Dynamin 1xA and Syndapin 1 form liquid-like condensates at synapses, which facilitate ultrafast endocytosis by enabling molecular crowding and intermolecular interactions.

This study shows FMRP is essential for activity-dependent bulk endocytosis in neurons, and targeting this process may alleviate hyperexcitability in fragile X syndrome.

This study shows that the SV2A-Syt1 interaction forms surface nanoclusters, which regulate their entry into recycling synaptic vesicles.