Erik Jorgensen (U. Utah / HHMI) 2: Recycling synaptic vesicles: Ultrafast endocytosis

www.ibiology.org/neuroscience...
Part 1: Synaptic Transmission: Jorgensen describes the historic experiments in electrophysiology and microscopy that led to our current understanding of synaptic transmission.
Part 2: Recycling Synaptic Vesicles: Ultrafast Endocytosis: Two mechanisms exist for recycling synaptic vesicles: clathrin-mediated and ultrafast endocytosis. Jorgensen explains why we need both.
Talk summary:
In his first talk, Dr. Jorgensen describes the historic experiments leading to our current understanding of synaptic transmission. In the 1950s, Sir Bernard Katz proposed that stimulation of a neuron caused synaptic vesicles to fuse with the plasma membrane and release neurotransmitter. Two decades later, John Heuser and Tom Reese produced stunning electron micrographs proving that Katz’ theory was right. In addition, Heuser and Reese made that surprising finding that just 30 sec after nerve stimulation, synaptic vesicles are recycled via clathrin-mediated endocytosis.
Part 2 of Jorgensen’s talk focuses on work from his lab showing that there is a second mechanism for recycling synaptic vesicles which he calls ultrafast endocytosis. Ultrafast endocytosis occurs 1000x faster that the clathrin-mediated endocytosis identified by Heuser and Reese. Using electron microscopy, Jorgensen and his colleagues found that non-clathrin mediated endocytosis begins so rapidly after stimulation that it overlaps in time with synaptic vesicle exocytosis! Jorgensen goes on to explain why two mechanisms for recycling synaptic vesicles are necessary in vivo.
Speaker Biography:
Erik Jorgensen is a Distinguished Professor of Biology and a member of the Program in Neuroscience at the University of Utah, and an Investigator of the Howard Hughes Medical Institute. His lab studies the molecular mechanisms of synaptic transmission with a focus on synaptic vesicle fusion and recycling. Jorgensen’s lab uses genetics, biochemistry, light and electron microscopy to investigate neurotransmission, primarily in C. elegans.
Jorgensen has been honored with the Utah Governor’s Medal for Science and Technology, a Humboldt Research Award from the Humboldt Foundation and he was one of the inaugural recipients of the F.R. Lillie Research Innovation Award from the Marine Biological Laboratory and the University of Chicago. Jorgensen has also received several awards for excellence in teaching from the University of Utah.
Jorgensen received his BS from the University of California, Berkeley and his PhD from the University of Washington. He was a postdoctoral fellow in the lab of H. Robert Horvitz at the Massachusetts Institute of Technology.
Learn more about Jorgensen’s research here:
biologylabs.utah.edu/jorgensen...
or here:
www.hhmi.org/scientists/erik-m...

[@nirjharaloy6108]

Thanks Dr. Jorgensen! This is amazing! The selection between slow and ultra fast recycling wasn't clear through our conventional lectures.

[@camilocastelblanco2903]

Fantastic talk! Thanks Dr. Jorgensen!

[@nathanrossen6904]

Thanks for the great lecture

[@chimerathirteen7057]

could it just be that ultrafast endocytosis doesn't occur at low temperatures and the only way to create synaptic vesicles is from clathrin mediated endocytosis since there is a lack of endocytic vesicles in the cell?

[@fips001]

isn't that exactly what he is saying?

[@chimerathirteen7057]

fips001 no, his hypothesis is that clathrin mediated endocytosis occurs when the neuron is over stimulated. Overstimulation is the stress condition he stated, not cold stress.

[@fips001]

both, look at 27:00

[@chimerathirteen7057]

Well not exactly. Yes he is stating that ultrafast endocytosis doesn't occur at the low temperatures. He then goes on to hypothesize why he doesn't see clathrin mediated endocytosis at 34C and hypothesizes that it will occur during overstimulation. It was the latter point I was addressing, not the 'how' but the 'why'.
My bad, I guess I wasn't being too clear in my statement - I think the hypothesis can be generalized. It seems to me that under any condition where ultrafast endocytosis doesn't occur, clathrin mediated endocytosis would take over. Why is simple - there aren't any endosomes containing neurotransmitters in the cytosol for the clathrin to take apart and regenerate the synaptic vesicle pool. In this situation the only thing clathrin would recognize instead of the endosome surface is the cytosolic face of the plasma membrane at the active zone, which would have a similar composition to the endosome surface.