An unexpected finding on how nerve cells signal to one another could rewrite the textbooks on neuroscience, says a collaborative team of researchers at Weill Cornell Medical College and Yale University.
Their study, published as a high-profile research article in the journal Science, suggests that a key cellular enzyme called dynamin 1 is not essential to all synaptic transmission, as experts had previously assumed.
Dynamin has long been a focus of research for its role in packaging chemical signals, called neurotransmitters, into tiny synaptic vesicles within the cell.
The new study finds that the enzyme is not always necessary for this process. Instead, dynamin 1 goes into action only when the synapse enters moments of especially high activity.
'In that sense, dynamin 1 remains crucial, allowing the synapse the freedom to function under all conditions,' explains co-senior author Dr. Timothy Ryan, professor of biochemistry at Weill Cornell Medical College.
The discovery is a potentially important new piece of the puzzle for scientists investigating neurological injury and disease.
'In the long run, what we're trying to achieve here is a kind of biochemical repair manual' for the brain and brain cells,' Dr. Ryan explains. 'So, in the future, if we find out that a particular illness is caused by a flaw in dynamin 1 function or proteins that interact with dynamin 1, we'll have answers on hand to help fix that.'
Dynamin 1 is one of a family of enzymes involved in synaptic vesicle endocytosis a reverse of the process of transmission of cellular signaling chemicals, whereby molecular components of the vesicle are retrieved from the synapse surface and fit back into a new vesicle to be recycled for reuse after the vesicle has discharged its neurotransmitter. One of the steps in this recycling is a biochemical process called fission.
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