NEW YORK (Dec. 20, 2007) -- At its core, healthy neurological function hinges on the efficient passage of information between brain cells via the synapse.
Figuring out how the synapse traffics this information -- a process called neurotransmission -- is crucial to understanding the function of the healthy and diseased brain.
Now, a team led by researchers at Weill Cornell Medical College in New York City has spotted a crucial new piece to that puzzle.
Their findings, published today in Neuron, focus on the role of a cellular enzyme called Synaptojanin 1 (Synj1).
Prior research had suggested the enzyme was key to certain late steps in the synaptic vesicle cycle, a critical aspect of synaptic function. But the new study finds that removing synj1 from the synapse dramatically slows one of the very first steps in the vesicle cycle in a process known as endocytosis.
"By disabling synj1 activity at key points, we effectively slowed endocytosis. That suggests this enzyme is far more important than we had ever assumed before," says study senior author Dr. Timothy A. Ryan, professor of biochemistry at Weill Cornell Medical College.
Here's how endocytosis works: Within brain cells, information is stored as electrical signals. However, before that information can be passed cell-to-cell, it must first be converted at the cell's surface into chemical signals that flow via the synapse.
Each synaptic transmission involves the carriage of a packet, or "vesicle," of neurotransmitter chemicals. Each synapse has only about 100 of these packets.
"Endocytosis involves the shuttling back and forth of these sac-like objects from the cell surface to the cell interior," Dr. Ryan says. When a vesicle empties, it isn't discarded, however. Instead, it undergoes complex chemical changes that enable it to be recycled and readied for another run.
Chemical signaling is crucial to this recycling process, and t
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New York- Presbyterian Hospital/Weill Cornell Medical Center/Weill Cornell Medical College