Mike-Cousin

#IDIBELLseminars: Function and dysfunction of synaptic vesicle endocytosis in physiology and disease

Michael Cousin

Centre for Discovery Brain Sciences

06/03/2026

13:00-14:00

Aula Taronja

Abstract

Synaptic vesicle (SV) endocytosis is essential to sustain neurotrasmission in mammalian brain. It performs this role in response to a wide range of physiological stimuli. During intense neuronal activity, activity-dependent bulk endocytosis (ADBE) is the dominant synaptic vesicle endocytosis mode, with glycogen synthase kinase 3 emerging as a key regulatory molecule. This seminar will present evidence for this role, specifically in the control of the lipid kinase phosphatidylinositol 4-kinase IIα.
Dysfunctional SV endocytosis is emerging as key determinant in a series of monogenic epilepsies. This seminar will focus on the role of pathogenic mutations in the large GTPase dynamin in epilepsy, and reveal potential theraputic interventions to correct SV endocytosis and the outcomes of its dysfunction.

Hosted by Tania López – Physiology and pathology of the functional relationship between glia and neurons group

Short Bio

Mike Cousin was awarded a BSc in Biochemistry from Edinburgh University and PhD in Biochemistry from Dundee University. He then won two fellowships (Royal Society and Human Frontiers of Science) to research synaptic vesicle endocytosis at the Children’s Medical Research Institute, Sydney, Australia. He returned to Edinburgh in 2000 to take up a lectureship position. He became Chair of Neuronal Cell Biology in 2010, and has been Co-Director of the Muir Maxwell Epilepsy Centre since 2013 and Co-Director of the Centre for Discovery Brain Sciences. He recently stepped down as Chair of the Scientific Advisory Committee of the Epilepsy Research Institute UK.
His research is focussed on the mechanisms that sustain neurotransmitter release across the range of neuronal activity. Specifically, he investigates the molecular mechanism of synaptic vesicle endocytosis modes and how synaptic vesicle cargo is retrieved during these events. This knowledge has been leveraged into determining the presynaptic contribution to a series of neurodevelopmental disorders, with a particular emphasis on monogenic epilepsy.

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